Open Access
ARTICLE
Yiren Jiao1,*, Lingbo Cao2, Jing Xu1, Hongkai Sun1, Jia Shi3, Xiaoli Ma1, Zehao Wang1,*, Baozhen Zhou1,*
BIOCELL, DOI:10.32604/biocell.2026.083738
Abstract Background: The inhibitor of MyoD family (Mdfi) has been characterized as a myogenic repressor that regulates transcription factor activity through cytoplasmic retention; however, its specific function in myoblast proliferation remains poorly understood. This study aimed to elucidate the precise role of Mdfi in regulating myoblast cell cycle progression and proliferation using the clustered regularly interspaced short palindromic repeat (CRISPR)/CRISPR-associated protein 9 (Cas9)-mediated gene editing. Methods: We employed the CRISPR/Cas9 system to construct Mdfi-knockout (Mdfi−/−) C2C12 cell lines. Cell cycle distribution was analyzed by flow cytometry, proliferation was assessed by EdU incorporation assays, and molecular mechanisms were investigated through… More >
Open Access
REVIEW
Hiromasa Tsuda1,2,*, Daichi Horikoshi3, Yoshikazu Mikami4
BIOCELL, DOI:10.32604/biocell.2026.081392
（This article belongs to the Special Issue: Cellular and Molecular Mechanisms of Gut Microbiota, Oxidative Stress, and Inflammation in Health and Disease)
Abstract Plaque-derived short-chain fatty acids (SCFAs) have emerged as potential contributors to periodontal inflammation and tissue destruction. Gram-negative anaerobic dental plaque bacteria produce millimolar concentrations of SCFAs. SCFAs directly affect gingival epithelial cells and infiltrating neutrophils, inducing membrane-disruptive cell death accompanied by the release of damage-associated molecular patterns, which can cause inflammation. In neutrophils, this process is also associated with the extracellular release of peptidyl-arginine deiminase 4 (PAD4) and citrullinated proteins, suggesting a potential link between periodontal inflammation and rheumatoid arthritis and cardiovascular disease. This review summarizes current knowledge on the mechanisms of SCFA-induced cell death More >
Open Access
REVIEW
Carlo Acierno1,*, Flavia Carriero2, Alfredo Caturano3, Valentina Rubino4, Ferdinando Carlo Sasso5, Salvatore D’Angelo2,6, Luca Rinaldi7, Giuseppe Terrazzano2
BIOCELL, DOI:10.32604/biocell.2026.085405
（This article belongs to the Special Issue: Cellular and Molecular Mechanisms of Gut Microbiota, Oxidative Stress, and Inflammation in Health and Disease)
Abstract Systemic infections expose the liver to convergent microbial, inflammatory, vascular, and metabolic stress signals. This narrative review synthesizes how hepatic immunometabolic reprogramming links innate immune sensing, bioenergetic stress, and sepsis-associated liver injury or dysfunction. It focuses on hepatocytes, Kupffer cells, liver sinusoidal endothelial cells, and hepatic stellate cells as a coordinated sinusoidal network rather than isolated cell compartments. Infection-derived pathogen-associated molecular patterns, host-derived damage-associated molecular patterns, cytokines, hypoxia, altered substrate flux, mitochondrial injury, endoplasmic reticulum stress, lipid remodeling, and redox imbalance are integrated into a temporal framework. Early responses may support host defense through acute-phase More >
Open Access
REVIEW
Takafumi Nakano1,*, Mayuka Morimoto-Arimatsu2,3, Kenichi Mishima2
BIOCELL, DOI:10.32604/biocell.2026.085207
（This article belongs to the Special Issue: Cellular and Molecular Insights into Brain Ischemic Insults)
Abstract Haptoglobin (Hp) is an acute-phase protein that binds free hemoglobin and limits hemoglobin-mediated oxidative injury. In addition to this established function, Hp modulates inflammatory responses and interacts with high-mobility group box 1 (HMGB1), a major damage-associated molecular pattern, suggesting a multifunctional role. Hp is primarily produced by the liver, although local expression in brain-resident cells has also been reported, potentially contributing to tissue-specific protection. This review summarizes the biological properties of Hp, including hemoglobin clearance, immune modulation, and HMGB1 scavenging, and discusses experimental and clinical evidence linking Hp to ischemic stroke. In acute ischemic stroke,… More >
Open Access
REVIEW
Hao Zhou1,2, Jianlin Zhou3, Lin Zhou1,2,*
BIOCELL, DOI:10.32604/biocell.2026.084272
（This article belongs to the Special Issue: Epigenetic and ncRNA Biomarkers in Cancer: Diagnostic and Prognostic Value)
Abstract Small nucleolar RNA host genes (SNHGs) generate both long non-coding RNAs and small nucleolar RNAs from the same primary transcripts. Among the 32 identified members, SNHG1 is the most extensively studied and primarily acts as an oncogene. This review adopts a mechanism-driven approach to systematically examine SNHG1 dysregulation and its roles in cancer. Specifically, we address: (1) how SNHG1 is transcriptionally and post-transcriptionally dysregulated in tumors; (2) the molecular mechanisms by which it regulates gene expression, including epigenetic mechanisms (histone modifications, DNA methylation), transcriptional regulation, post-transcriptional regulation (mRNA stability, microRNA sponging), and protein-level regulation; and More >
Open Access
ARTICLE
Pin-Si Yin1,#, Chang-Chin Wu1,2,#, Shih-Yuan Chiu1, Karina Erda Saninggar3, Ardianti Maartrina Dewi3, Kai-Chiang Yang1,3,4,*
BIOCELL, DOI:10.32604/biocell.2026.081934
（This article belongs to the Special Issue: Unraveling Periodontal Disease: Molecular and Cellular Perspectives)
Abstract Objective: Periodontal diseases can cause pro-inflammatory cytokine overproduction, particularly tumor necrosis factor-alpha (TNF-α), and this inflammatory microenvironment is a critical driver of oral cancer progression. MicroRNA-146a-5p is a key regulator of inflammation, linked to both periodontal disease and carcinogenesis. The objective of this study was to illustrate the regulatory function of miR-146a-5p in gingival squamous cell carcinoma OECM-1 cells under conditions that mimic those of periodontal disease. Methods: OECM-1 cells were stimulated with 25 ng/mL TNF-α for 48 h, and subsequently transfected with 50 nM miR-146a-5p mimic or inhibitor for an additional 48 h. The inflammatory… More >
Open Access
REVIEW
Andrzej Grzybowski1,2,*, Aušrinė Bajoriūnaitė3, Reda Žemaitienė3
BIOCELL, DOI:10.32604/biocell.2026.083756
（This article belongs to the Special Issue: Modulation of Inflammation, Oxidative Stress, and Mitochondrial Function: Therapeutic Perspectives Across Diseases)
Abstract Oxidative stress results from an imbalance between reactive oxygen species (ROS) production and antioxidant defense mechanisms and contributes to cellular damage and the pathogenesis of various diseases. This review summarizes recent advances in the molecular and biochemical mechanisms associated with oxidative stress in ocular diseases, including dry eye disease, diabetic retinopathy, age-related macular degeneration (AMD), glaucoma, and cataract. A literature search was conducted using PubMed and Google Scholar databases to identify relevant studies published up to 31 December 2025. Current evidence suggests that oxidative stress plays an important role in inflammation, mitochondrial dysfunction, and cellular More >
Open Access
ARTICLE
Lu Yang1,#, Man Tian2,#, Jinyue Zhu1,*
BIOCELL, DOI:10.32604/biocell.2026.082951
Abstract Background: Macrophage-derived eicosanoids are involved in airway inflammation associated with asthma, but the mechanisms regulating their production remain incompletely understood. The study aimed to evaluate the effects of isorhynchophylline (IRN) on eicosanoid production and inflammatory activation in LPS/IFN-γ-stimulated THP-1-derived macrophages and to further investigate whether these effects are mediated through the miR-200a/FOXC1/NF-κB axis. Methods: THP-1 cells were differentiated into M0 (PMA) and polarized into M1 (LPS+IFN-γ) phenotypes. IRN (5–20 μM) was applied. Eicosanoids (PGE2, LTB4) were measured via ELISA; COX-2, 5-LOX, mPGES-1, FOXC1, p-IκBα/IκBα, and p-p65/p65 were measured via Western blotting; and miR-200a and target genes were… More >
Open Access
REVIEW
Milena Rašeta, Sanja Djokić, Sladjana Stanisavljević, Jelena Tadić, Marija Lesjak, Nataša Simin, Nemanja Živanović*
BIOCELL, DOI:10.32604/biocell.2026.084885
Abstract Parkinson’s disease (PD) is a progressive neurodegenerative disorder marked by dopaminergic neuronal loss, mitochondrial impairment, neuroinflammation, and excessive oxidative stress. The transcription factor nuclear factor erythroid 2–related factor 2 (Nrf2) plays a central role in maintaining cellular redox balance and regulating cytoprotective gene expression, positioning it as an attractive therapeutic target in PD. A growing body of evidence highlights that diverse natural products, including polyphenols, alkaloids, lactones, polyamines, terpenoids, and related secondary metabolites, can modulate Nrf2 signaling and confer neuroprotection. This review provides a comprehensive and updated overview of these compounds, focusing on their molecular More >
Open Access
REVIEW
Stephanie Seneff1,*, Anthony M. Kyriakopoulos2,3
BIOCELL, DOI:10.32604/biocell.2026.084346
（This article belongs to the Special Issue: Autophagy and Oxidative Stress in Cancer: Molecular Crossroads and Cell Fate Decisions)
Abstract It is increasingly becoming recognized that cancer is primarily a metabolic disease, as manifested by the Warburg effect. Cancer cells exploit their mitochondria to convert the intermediates in the citric acid cycle into resources to support rampant proliferation. Our team has published research claiming that systemic deuterium overload in mitochondria is a risk factor for cancer. Deuterium (heavy hydrogen) is toxic to the F1F0-ATP synthase nanomotors in the mitochondria that produce ATP, the energy currency of the cell. Over time, cancer cells become resistant to chemotherapy, and, paradoxically, the resident stromal cells and immune cells assist… More >
Graphic Abstract
Open Access
REVIEW
Alexandra Popa1,2, Alexandra Ripszky1,2,*, Sebastian Andrei Bancu1,2, Melis Izet1, Radu Vasile Radulescu2,*, Florentina Rus2, Ecaterina Andronescu3,4, Ana Cernega5, Silviu Mirel Pituru5
BIOCELL, DOI:10.32604/biocell.2026.084761
（This article belongs to the Special Issue: Autophagy and Oxidative Stress in Cancer: Molecular Crossroads and Cell Fate Decisions)
Abstract Periapical lesions (PAL) are chronic inflammatory conditions resulting from microbial invasion of the root canal system. Despite available treatments, failure rates of 20–35% highlight the need for a deeper understanding of their molecular mechanisms. This review provides an in-depth look at three interconnected cellular processes—oxidative stress, autophagy, and apoptosis—and examines their roles in PAL development and progression. Reactive oxygen species (ROS) activate redox-sensitive signaling pathways such as NF-κB, the Keap1–Nrf2/ARE axis, and MAPK cascades, disrupting bone homeostasis by inhibiting osteoblast formation and enhancing osteoclast activity via the RANKL–RANK–OPG pathway. Cell survival or death during inflammation More >
Open Access
REVIEW
Wojciech Łukowski*
BIOCELL, DOI:10.32604/biocell.2026.081112
Abstract Type 1 diabetes (T1D) is traditionally described as a T cell–mediated autoimmune disease, yet accumulating longitudinal evidence indicates that metabolic and environmental perturbations—including depletion of short-chain fatty acid (SCFA)–producing gut microbiota—precede seroconversion and overt autoimmunity. We propose that SCFA loss represents an upstream trigger of endocannabinoid system (ECS) imbalance in T1D. Integrating evidence from microbiome, lipid signaling, mitochondrial biology, and immunometabolic research, we construct a mechanistic model in which reduced SCFA availability impairs lipid homeostasis and promotes overproduction of 2-arachidonoylglycerol (2-AG), potentially driving cannabinoid receptor 1 (CB1) dominance and receptor asymmetry. The resulting arachidonic acid More >
Open Access
ARTICLE
Yuqing Kang#, Jiangbo Zheng#, Chunyan Mou#, Ranxu Lv, Xing Xue*
BIOCELL, DOI:10.32604/biocell.2026.081318
（This article belongs to the Special Issue: Advanced Cell Signaling Pathways in Health and Disease)
Abstract Objectives: Tumor-associated macrophages (TAMs) within the hypoxic tumor microenvironment critically drive colorectal cancer (CRC) progression, yet their specific regulatory mechanisms on endoplasmic reticulum (ER) homeostasis via microRNAs remain understood. This study aims to assess the impact of hypoxia-induced TAMs on CRC cells through the microRNA-320 (miR-320)/SRY-box transcription factor 4 (SOX4) axis, focusing on ER homeostasis and malignant behaviors. Methods: Human CRC cell lines HCT116 and SW480 were co-cultured with hypoxia-induced macrophages. Cells were treated with miR-320 mimics and inhibitors to evaluate proliferation and apoptosis using Cell-counting kit-8 (CCK8) assays and flow cytometry. Western blotting was performed… More >
Open Access
REVIEW
Patrycja Obrycka1,*, Nikodem Oślizło2, Agnieszka Frątczak1, Maja Ickiewicz1, Patrycja Paszenda1, Jasmin Sobala1, Julia Soczyńska1, Sławomir Woźniak3
BIOCELL, DOI:10.32604/biocell.2026.084626
（This article belongs to the Special Issue: Gut Microbiota-Derived Molecules and Cellular Mechanisms in Host Health and Disease)
Abstract Growing evidence indicates that the gut–brain axis plays a central role in cognitive regulation, with microbial metabolites acting as important mediators of neuronal function. This review examines how postbiotics—bioactive compounds produced by microorganisms, including short-chain fatty acids, indole derivatives, bacterial peptides, and extracellular vesicles—may influence memory-related processes and cognitive resilience. Particular attention is given to the molecular and intracellular mechanisms through which postbiotics interact with host targets, including G-protein–coupled receptors, the aryl hydrocarbon receptor, and epigenetic regulators. Activation of these pathways modulates signaling cascades such as mitogen-activated protein kinase/extracellular signal-regulated kinase (MAPK/ERK), phosphoinositide 3-kinase/protein kinase More >
Open Access
REVIEW
Carlo Acierno1,*, Flavia Carriero2, Alfredo Caturano3, Ferdinando Carlo Sasso4, Salvatore D’Angelo5,6, Luca Rinaldi7, Giuseppe Terrazzano2
BIOCELL, DOI:10.32604/biocell.2026.084065
（This article belongs to the Special Issue: Cellular and Molecular Mechanisms of Gut Microbiota, Oxidative Stress, and Inflammation in Health and Disease)
Abstract Microbiota-derived metabolites have emerged as modulators of hepatic redox biology, because the liver is the first organ to receive and biotransform gut-derived signals through the portal circulation. Oxidative stress is best viewed as a dynamic, compartmentalized redox network rather than a static excess of reactive species. This review provides a liver-centered, mechanistic synthesis of how microbiota-derived products influence hepatic redox balance through receptor sensing, first-pass biotransformation, immunometabolic remodeling, and subcellular stress responses. Particular attention is given to direct microbial metabolites (short-chain fatty acids, indoles, and aromatic derivatives), the trimethylamine/trimethylamine N-oxide axis, bile acid pool remodeling,… More >
Open Access
REVIEW
Yongfeng Li1, Peirong Tian2, Jieqian Zheng2, Yingying Cui2, Limei Gao2,*
BIOCELL, DOI:10.32604/biocell.2026.083591
（This article belongs to the Special Issue: Bioactive Natural Components as Regulators of Cellular Pathways and Disease Progression)
Abstract Melatonin (N-acetyl-5-methoxytryptamine, Mel) is a small indole hormone molecule widely distributed in almost all living organisms, and it has multiple biological functions. Currently, melatonin has been reported to play a positive regulatory role in growth and development modulation, circadian rhythm conversion, antioxidant metabolism, plant immunity, cell senescence, and photosynthetic energy conversion for higher plants. This article systematically expounds the research progress of melatonin on the transcriptional regulation of photosynthesis-related genes, the structure and function of photosynthetic proteins, photosynthate metabolism, chloroplast ROS metabolism, and biological rhythms in higher plants, and then summarizes the hot issues and More >
Open Access
REVIEW
Dina Tenji1, Nina Tomić2, Marija Petrović3, Marina Jovanović3,*
BIOCELL, DOI:10.32604/biocell.2026.083171
（This article belongs to the Special Issue: Advances in Nrf2 Signaling Pathway in Neurodegenerative Diseases)
Abstract The transcription factor nuclear factor erythroid 2-related factor 2 (Nrf2) is a central regulator of cellular defense mechanisms. It coordinates antioxidant responses, redox homeostasis, inflammation control, mitochondrial function, intracellular iron dynamics, glucose metabolism, lipid metabolism, and proteostasis. Dietary polyphenols can effectively modulate Nrf2 by directly activating the Kelch-like ECH-associated protein 1 (Keap1)-Nrf2-antioxidant response elements (ARE) pathway and by indirectly influencing upstream kinases, epigenetic processes, and metabolites produced by the gut microbiota. By-products, generated in large quantities by the beverage industries, represent an abundant yet underexploited source of polyphenol-rich bioactive compounds. This narrative review critically summarizes More >
Open Access
ARTICLE
Zhuyuan Ren, Yong Chen, Jiaqiao Wu, Qiang Li, Qiang Fu*
BIOCELL, DOI:10.32604/biocell.2026.085300
Abstract Background: Volatile anesthetics such as sevoflurane are ubiquitous in perioperative care, yet their unintended consequences on pulmonary microvascular integrity and the upstream intracellular signaling pathways remain incompletely defined. This study elucidates the precise transcriptional mechanisms linking sevoflurane exposure to pulmonary endothelial hyperpermeability. Methods: Transendothelial electrical resistance (TEER) and macromolecular permeability were dynamically quantified in human pulmonary microvascular endothelial cell (HPMEC) monolayers following sevoflurane exposure. Global transcriptomic profiling (RNA-seq) was employed to identify core regulatory nodes, which were functionally validated via targeted siRNA silencing in vitro and subsequently corroborated in a murine model of clinical sevoflurane inhalation. Results: Sevoflurane… More >
Open Access
REVIEW
Federica Armeli*, Beatrice Mengoni, Maria Luisa Crudeli, Martina Menin, Rita Businaro
BIOCELL, DOI:10.32604/biocell.2026.084039
（This article belongs to the Special Issue: Advances in Nrf2 Signaling Pathway in Neurodegenerative Diseases)
Abstract Neurodegenerative diseases represent a growing global challenge linked to aging, sharing core pathogenic mechanisms such as oxidative stress, neuroinflammation, and mitochondrial decay. This review evaluates the neuroprotective potential of specific polyphenols and carotenoids in modulating key signaling pathways. These nutraceuticals promote the nuclear translocation of Nrf2, the master regulator of antioxidant defenses, while simultaneously inhibiting the NF-κB pathway to suppress pro-inflammatory cytokine production. By facilitating the microglial switch from neurotoxic to neuroprotective phenotype, these bioactive compounds effectively break the cycle of chronic neuronal damage. While these molecules offer a promising non-invasive strategy to delay disease progression, More >
Open Access
REVIEW
José Manuel Pérez de la Lastra1,*, Celia María Curieses Andrés2, Elena Bustamante Munguira2, Celia Andrés Juan3, Eduardo Pérez Lebeña4
BIOCELL, DOI:10.32604/biocell.2026.080868
Abstract Nuclear factor erythroid 2-related factor 2 (NRF2) orchestrates antioxidant defence, electrophile detoxification, and stress recovery across tissues. This paper frames chronic disease vulnerability through the lens of NRF2 insufficiency, defined as reduced functional output of the antioxidant response element programme. We describe the mechanisms that blunt NRF2 signalling, including genetic variation in NFE2L2 and Keap1, epigenetic repression, post-translational degradation routes, and cumulative exposome pressures. Downstream consequences include impaired glutathione-centred buffering, mitochondrial dysfunction, proteostasis failure, inflammatory amplification, and heightened susceptibility to regulated cell death. Using an organ-by-endotype approach, we map recurring patterns across lung, liver, and More >
Open Access
REVIEW
Yuhua Chen1,#, Xianyi Tan1,#, Yansong Hu1, Ye Tang1, Zhengbao Zhang1,*, Shengkui Tan2,3,4,*, Xiaonian Zhu1,*
BIOCELL, DOI:10.32604/biocell.2026.084419
Abstract Per- and polyfluoroalkyl substances (PFAS) are widely used in industrial processes because of their unique physicochemical properties. Mitochondria—double-membrane organelles present in most eukaryotic cells—govern cellular fate by maintaining structural integrity and bioenergetic homeostasis. Recent studies have demonstrated that PFAS can impair mitochondrial ultrastructure, disrupt energy metabolism, elicit oxidative stress, and trigger mitochondria-dependent apoptotic signaling, potentially contributing to reproductive and developmental disorders, hepatic dysfunction, neurotoxicity, and cardiovascular injury. Therefore, mitochondrial damage may represent one mechanistic pathway contributing to PFAS-associated adverse health outcomes. Here, we summarize current knowledge of the effects of PFAS exposure on mitochondrial architecture More >
Open Access
REVIEW
Ziyi Guo, Zhenkai Wang, Zixuan Song, Tian Wang, Jingai Fang, Ziyuan Zhang*
BIOCELL, DOI:10.32604/biocell.2026.083188
（This article belongs to the Special Issue: Cellular Senescence in Health and Disease)
Abstract Chronic kidney disease (CKD) poses a significant global health challenge, with the accumulation of senescent cells contributing to its pathogenesis. This review synthesizes recent advances highlighting mitochondrial dysfunction as a pivotal driver of cellular senescence in CKD progression. We delineate how CKD-specific pathological insults—such as uremic toxins and metabolic stress—compromise mitochondrial integrity, triggering a cascade of interconnected failures: dysregulation of mitochondrial quality control (impaired biogenesis via PGC-1α suppression, disrupted dynamics, and deficient mitophagy) leads to the persistence of damaged organelles. Concurrent bioenergetic decline from compromised oxidative phosphorylation and elevated reactive oxygen species (ROS) production further More >
Open Access
ARTICLE
Zhikai Wang1, Xing Wang2, Lun Dong1, Wei Wang1, Xiaoping Gao1,*
BIOCELL, DOI:10.32604/biocell.2026.081668
Abstract Objectives: Middle ear cholesteatoma (MEC) is a destructive and locally invasive disease that leads to erosion of bone structure and serious complications. This study aimed to investigate the role of GDF11 in promoting the differentiation of macrophages into osteoclasts in vitro and elucidate the bone erosion mechanism in MEC. Methods: The MEC dataset GSE116142 was subjected to bioinformatics analysis. The Growth Differentiation Factor 11 (GDF11) and Transforming Growth Factor Beta Receptor 1 (TGFBR1) expression levels in MEC were evaluated using immunohistochemical analysis. RAW264.7 cells were induced with different concentrations of recombinant GDF11 (rGDF11) with or without the… More >
Open Access
ARTICLE
Akash S. Mali1, Debanjan Das2, Denise Greco1, Petr Telensky1, Jiri Novotny1,*
BIOCELL, DOI:10.32604/biocell.2026.080886
Abstract Background: Opioids can modulate mitochondrial redox homeostasis and autophagy and are implicated in the regulation of key physiological and pathological processes, including aging, cellular metabolism, and tumorigenesis. The study aimed to investigate how opioid receptor agonists influence lipopolysaccharide-induced senescence in microglia. Methods: C8-B4 microglial cells were either left untreated or pretreated with different opioid agonists and subsequently exposed to lipopolysaccharide (LPS). Colorimetric assays, fluorescence microscopy, flow cytometry, and Western blotting were used to assess cellular senescence, autophagy-associated changes, reactive oxygen species, and calcium levels, as well as the expression of selected marker proteins and signaling molecules. Results:… More >
Graphic Abstract
Open Access
REVIEW
Carmen Rubio1,#, Norma Serrano-García1,#, Ángel Lee2, Javier Pérez-Villavicencio1,3, Omar Villa-Robledo1,4, Rodrigo Mercado Pimentel5, Héctor Romo-Parra1,6, Moisés Rubio-Osornio7,*
BIOCELL, DOI:10.32604/biocell.2026.081478
（This article belongs to the Special Issue: Transporters and Channels in Brain Physiology: From Molecular Biophysics to Cellular Dynamics)
Abstract Epilepsy is sustained by a self-reinforcing triad of ion channel dysfunction, mitochondrial impairment, and oxidative stress that lowers seizure threshold and drives epileptogenesis. This review examines how genetic channelopathies and redox-dependent post-translational modifications of voltage-gated sodium, calcium, and potassium channels disrupt excitatory–inhibitory balance, and how electron transport chain dysfunction amplifies reactive oxygen species, compromises adenosine triphosphate (ATP)-dependent membrane stability, and activates mechanistic target of rapamycin complex 1. Key convergences include oxidative ion channel modification, ATP-sensitive potassium channel impairment, synaptic lipid peroxidation, and gamma-aminobutyric acid (GABA)-ergic transporter dysfunction. Temporal lobe epilepsy is characterized by focal mitochondrial More >
Open Access
REVIEW
Hassan Ali1,2,3, Tsvetelina Velikova3,*, Petya Marinova3
BIOCELL, DOI:10.32604/biocell.2026.081372
（This article belongs to the Special Issue: Cellular and Molecular Mechanisms of Gut Microbiota, Oxidative Stress, and Inflammation in Health and Disease)
Abstract The gut microbiota, oxidative stress, and extracellular vesicles (EVs) form an interdependent triad essential for gastrointestinal homeostasis and systemic health. This narrative review summarizes the molecular crosstalk among these components in inflammation and disease. Literature was retrieved from PubMed and Scopus using relevant keywords and reference screening. Gut microbes regulate redox balance through metabolites such as short-chain fatty acids and modulation of host reactive oxygen species (ROS) production via mitochondrial pathways and nicotinamide adenine dinucleotide phosphate (NADPH) oxidase. Dysbiosis has been associated with excessive ROS generation, impaired antioxidant defenses, and activation of redox-sensitive signaling pathways,… More >
Open Access
REVIEW
Kimiya Ganjooi, Sophia Strukel, Emma Eddy, Ryan Au, Vikrant Rai*
BIOCELL, DOI:10.32604/biocell.2026.077955
（This article belongs to the Special Issue: Novel Targeted Therapy in Oncology)
Abstract Triple-negative breast cancer (TNBC) is defined by the absence of estrogen, progesterone, and human epidermal growth factor receptor 2 expression and exhibits significant molecular heterogeneity and aggressive clinical behavior. The main treatment remains traditional chemotherapy, despite the modest duration of its effects, which has intensified the search for novel, non-chemotherapeutic drugs. Over the past few years, various molecularly targeted and immune-based treatments targeting TNBC’s diverse oncogenic drivers have been uncovered. In immunotherapy, checkpoint blockade and chimeric antigen receptor (CAR)-T cells show growing promise, enabling selective tumor targeting with reduced off-target toxicity. Multi-omics investigations integrating genomic,… More >
Open Access
ARTICLE
Kristina Pilipović1,*, Lucia Fabijančić2, Iva Kristić1, Lara Saftić Martinović3
BIOCELL, DOI:10.32604/biocell.2026.079918
（This article belongs to the Special Issue: Cellular Mechanisms in Neurodegeneration, Injury, and Regeneration)
Abstract Objectives: Neuroinflammation, largely mediated by microglial activation, plays a central role in the pathogenesis of neurodegenerative diseases. In this study, we aimed to evaluate olive leaf extracts (OLEs) from three Croatian cultivars (Buža, Oblica, and Leccino) in the context of lipopolysaccharide (LPS)-induced activation of BV-2 microglia. Methods: Extracts were prepared by aqueous maceration and ethanol extraction under conditions compatible with downstream cell-culture use. Total phenolic and flavonoid contents were determined for both extract types, alongside targeted liquid chromatography–mass spectrometry (LC–MS/MS) quantification of major phenolic compounds. Based on compositional analysis, ethanolic extracts were selected for further evaluation,… More >
Open Access
REVIEW
Giuliana Colonna Soldavini1,2,#, María Belén Gomez1,#, Jeremias Martin Cuello1,2, Martín Gabriel Codagnone1,2, Analía Gabriela Reinés1,2,*
BIOCELL, DOI:10.32604/biocell.2026.082340
Abstract Astrocytes and microglia are key regulators of neuronal and synaptic function through dynamic interactions with neurons and with each other. Under pathological conditions, these interactions become dysregulated, promoting reactive glial states characterized by the release of pro-inflammatory cytokines, including IL-1β, TNF-α, and IL-6, as well as complement components such as C1q and C3, reactive oxygen species, and other inflammatory mediators that disrupt synaptic homeostasis and neuronal stability. In this review, we examine the molecular and cellular mechanisms underlying neuron-glia and astrocyte-microglia communication in physiological and neuroinflammatory conditions. We discuss how glial-derived factors influence synaptic remodeling, More >
Open Access
REVIEW
Shazia Ansari1, Gursimran Singh1, Jemimol Solomon1, Simranpreet Kaur1, Khadga Raj Aran1,2,*
BIOCELL, DOI:10.32604/biocell.2026.082358
（This article belongs to the Special Issue: Gut Microbiota-Derived Molecules and Cellular Mechanisms in Host Health and Disease)
Abstract Neurodegenerative diseases such as Alzheimer’s disease (AD), Parkinson’s Disease (PD), and Multiple sclerosis (MS) represent a growing global health burden characterized by progressive neuronal loss, chronic neuroinflammation, immune dysregulation, and metabolic dysfunction. Increasing evidence highlights the gut-brain-immune axis as a critical regulator of disease susceptibility and progression. Microbiota-derived short-chain fatty acids (SCFAs), including acetate, propionate, and butyrate, act as key postbiotic mediators that link intestinal microbial activity to the central nervous system. SCFAS modulates neurodegenerative pathways by regulating glial activation, inflammatory signaling, barrier integrity, and epigenetic and metabolic processes. Altered SCFAS production is consistently associated More >
Open Access
ARTICLE
Qianqian Peng, Fengjian He, Shumin Pan, Yinghua Ou*
BIOCELL, DOI:10.32604/biocell.2026.081188
Abstract Background: Nonalcoholic steatohepatitis (NASH) is a liver disease characterized by inflammation and fibrosis. Oridonin (Ori) exhibits anti-inflammatory and anti-fibrotic properties, but its role in NASH remains unclear. The study aimed to investigate whether Ori alleviates NASH injury by regulating pyroptosis through the nuclear factor-κB (NF-κB)/nucleotide-binding oligomerization domain-like receptor protein 3 (NLRP3) axis. Methods: An in vitro NASH model was established in HepG2 cells using free fatty acids (FFA), and an in vivo model was induced in mice using a methionine-choline-deficient (MCD) diet. Biochemical assays, staining, flow cytometry, Western blot, and immunofluorescence assessed lipid accumulation, oxidative stress, inflammation, pyroptosis,… More >
Graphic Abstract
Open Access
CORRECTION
Jinni Ma#, Meilin Zhou#, Xin Xu, Xinyao Gao, Haixia Wang, Jinhua Shen, Lu Xue*
BIOCELL, DOI:10.32604/biocell.2026.085899
Abstract This article has no abstract. More >
Open Access
REVIEW
José Manuel Pérez de la Lastra1,*, Celia María Curieses Andrés2, Elena Bustamante Munguira2, Celia Andrés Juan3, Eduardo Pérez-Lebeña4
BIOCELL, DOI:10.32604/biocell.2026.080867
（This article belongs to the Special Issue: Advances in Nrf2 Signaling Pathway in Neurodegenerative Diseases)
Abstract Nuclear Factor Erythroid 2-Related Factor 2 (NRF2) and Nuclear Factor kappa B (NF-κB) are central regulators of redox balance and inflammation, and in healthy tissues, their activities are tightly coordinated. Classical models emphasise an antagonistic relationship in which NRF2-driven antioxidant programmes limit the oxidative cues that sustain NF-κB signalling, while inflammatory cascades can restrain cytoprotective responses when robust host defence is required. Increasing evidence from experimental systems and human tumours indicates that this antagonism is frequently relaxed in cancer. Chronic exposure to reactive oxygen species (ROS), cytokines, hypoxia, and mechanical distortion reconfigures the shared regulatory More >
Open Access
MINI REVIEW
Eui-Hwan Choi*
BIOCELL, DOI:10.32604/biocell.2026.079386
（This article belongs to the Special Issue: Autophagy and Oxidative Stress in Cancer: Molecular Crossroads and Cell Fate Decisions)
Abstract Peroxiredoxin 5 (PRX5) is an atypical 2-Cys peroxiredoxin distributed across mitochondria, peroxisomes, cytosol, and nucleus. Unlike other PRX isoforms, PRX5 acts not only as a reactive oxygen species (ROS) scavenger but also as a redox-dependent regulator of oncogenic signaling. Cancer stem cells (CSCs) maintain low intracellular ROS to preserve self-renewal and drug resistance, and PRX5 has emerged as a key mediator of this redox control. This review examines the. PRX5-ROS-Signal Transducer and Activator of Transcription 3 (STAT3) axis in CSC biology. We present mechanistic evidence demonstrating that PRX5-mediated redox balance protects STAT3 from oxidative inactivation More >
Open Access
REVIEW
Yi Lu1,#, Lixiang Wang1,#, Jiaheng Xu1,#, Heru Wang1, Jiayu Li1, Wanshun Li1, Xinyi Su1, Hongyu Li2, Deyu Zhang1,*, Zhendong Jin1,*, Haojie Huang1,*
BIOCELL, DOI:10.32604/biocell.2026.082978
Abstract Autophagy and oxidative stress form a bidirectional and dynamic regulatory network governing cell fate. Dysregulation of this crosstalk contributes to the pathogenesis of various diseases, including cancer, neurodegeneration, inflammation, metabolic disorders, and aging. Therefore, a deep understanding of the molecular mechanisms underlying the interplay between autophagy and oxidative stress provides a theoretical foundation for developing therapeutic strategies targeting this axis. This review synthesizes recent literature on the underlying molecular mechanisms. Oxidative stress drives autophagic initiation through multiple interconnected pathways, including direct oxidative modification of core autophagy-related proteins, modulation of canonical signaling cascades, activation of nuclear More >
Open Access
REVIEW
Kamila Grzelecka1, Julia Gałęziewska1,2, Weronika Kruczkowska1,2, Elżbieta Płuciennik1,*
BIOCELL, DOI:10.32604/biocell.2026.083009
（This article belongs to the Special Issue: Novel Targeted Therapy in Oncology)
Abstract Pyruvate kinase M2 (PKM2) is a central regulator of cancer metabolism, bridging metabolic reprogramming with oncogenic signaling and immune modulation. Unlike constitutively active PKM1, PKM2 displays structural and functional plasticity, allowing dynamic control of glycolytic flux while supporting anabolic processes associated with the Warburg effect. Beyond metabolism, PKM2 translocates to the nucleus, where it acts as a transcriptional coactivator and protein kinase influencing proliferation, angiogenesis, metastasis, redox balance, epigenetic remodeling, and therapeutic resistance. This review summarizes current knowledge on PKM2 as an immunometabolic regulator within the tumor microenvironment, focusing on immune cell polarization, metabolic competition, More >
Open Access
REVIEW
Yiting Zhao, Lei Gao*
BIOCELL, DOI:10.32604/biocell.2026.083060
Abstract Metformin is widely recognized for its pleiotropic effects on aging hallmarks, yet the evidence remains descriptive and mechanistically fragmented. This is a mechanism-focused narrative review; the evidence is illustrative rather than being systematically retrieved. We critically evaluate the proposed geroprotective mechanisms of metformin, including AMP-activated protein kinase activation (AMPK), mitochondrial complex I inhibition, senescence-associated secretory phenotype (SASP) suppression, and epigenetic modulation. While ample data support these pathways in preclinical models, resolving the relative contribution of these pathways requires: (i) locus-specific analysis of context-dependent H3K27me3 regulation (reported as both increased and decreased), and (ii) direct testing More >
Open Access
ARTICLE
Wentao Su1,#, Aishan Gulijiakela1,#, Jihao Xiong1, San Zhang1, Ke Ma2,*
BIOCELL, DOI:10.32604/biocell.2026.081235
（This article belongs to the Special Issue: Bioactive Natural Components as Regulators of Cellular Pathways and Disease Progression)
Abstract Objective: Mitochondrial dysfunction and ferroptosis contribute critically to acute lung injury (ALI), yet therapies targeting this pathway remain limited. This study investigates whether Salviadione, a rare alkaloid, protects against lipopolysaccharide (LPS)-induced epithelial damage by modulating the mitochondrial ferroptosis pathway. Methods: Network pharmacology, molecular docking, and molecular dynamics simulations identified potential targets. An in vitro model of lung epithelial injury was established using BEAS-2B cells exposed to LPS. Cell viability, lactate dehydrogenase (LDH) release, lipid peroxidation, Fe2+ accumulation, glutathione peroxidase 4 (GPX4) and acyl-CoA synthetase long-chain family member 4 (ACSL4) expression, mitochondrial membrane potential (ΔΨm), mitochondrial reactive oxygen species… More >
Open Access
ARTICLE
Liangliang Liu, Linjun Wang, Xin Song, Zhen Liu*
BIOCELL, DOI:10.32604/biocell.2026.080414
Abstract Background: Myocardial ischemia-reperfusion (I/R) injury represents a severe pathological process in cardiovascular diseases. This study aims to elucidate the mechanism of the yeast ovarian tumor (OTU) domain-containing protein 1 (YOD1) in cardiomyocyte injury. Methods: A hypoxia/reoxygenation (H/R) model was established using human AC16 cells to simulate I/R injury in vitro. Reverse transcription quantitative PCR (RT-qPCR) and western blotting were used to detect gene and protein expression. Cellular functions were evaluated using Cell Counting Kit-8 (CCK-8), lactate dehydrogenase (LDH), enzyme-linked immunosorbent assay (ELISA), flow cytometry, and biochemical kits. Protein interaction was validated through co-immunoprecipitation (Co-IP), ubiquitination assays, and… More >
Open Access
REVIEW
Rui Wang1,#, Fangyu Shi2,#, Bing Zhang3,*, Tiejun Wang3,*
BIOCELL, DOI:10.32604/biocell.2026.083727
（This article belongs to the Special Issue: MitoROS: Exploring Mitochondria and Oxidative Stress)
Abstract Placenta accreta spectrum (PAS) is a severe obstetric complication characterized by pathologically deep trophoblast invasion. Current clinical management relies heavily on reactive surgical interventions due to a lack of early predictive biomarkers and targeted therapies. This review proposes that the mitochondrion serves as the central metabolic-signaling hub driving PAS progression. We systematically analyze how mitochondrial metabolic reprogramming—specifically a Warburg-like shift toward glycolysis—and dysregulated quality control mechanisms promote maladaptive trophoblast phenotypic reprogramming. Central to this process is the “PAS-mitochondria-derived reactive oxygen species (MitoROS)” axis, where MitoROS species act as persistent signal amplifiers promoting epithelial-mesenchymal transition, apoptosis More >
Open Access
REVIEW
Alper Fatih Ardic1, Nurittin Ardic2,*
BIOCELL, DOI:10.32604/biocell.2026.082812
（This article belongs to the Special Issue: Cellular and Molecular Insights into Brain Ischemic Insults)
Abstract Neutrophil extracellular traps (NETs) are increasingly recognized as significant contributors to neurovascular damage following ischemic brain injuries. This review examines how NETs link intravascular thrombosis to downstream neuroinflammation via a pathway-centric framework. We synthesize recent preclinical and clinical evidence showing that NET-derived histones, extracellular DNA, and granular enzymes activate convergent inflammatory pathways, including the high mobility group box 1–Toll-like receptor 4 axis, nuclear factor kappa B, Janus kinase 2/signal transducer and transcription activator 3, NOD-like receptor pyrin domain-containing 3 inflammasome, and cyclic GMP–AMP synthase–interferon gene signaling. These mechanisms contribute to disruption of the blood-brain barrier, More >
Open Access
MINI REVIEW
Mi Ri Kim1, Ok-Hyeon Kim2, Hyun Jung Lee1,2,*
BIOCELL, DOI:10.32604/biocell.2026.081123
（This article belongs to the Special Issue: Advanced Cell Signaling Pathways in Health and Disease)
Abstract Aging and brain injury remodel the central nervous system (CNS) physical microenvironment, yet the contribution of these mechanical changes to neurodegenerative disease remains underappreciated. While traditional models emphasize biochemical mechanisms, emerging evidence indicates that altered tissue stiffness, extracellular matrix composition, and interstitial fluid dynamics actively reprogram intracellular signaling via dysregulated mechanotransduction. This review describes key physical cues shaping the brain microenvironment, including substrate rigidity and fluid flow within the cerebrospinal fluid (CSF) and glymphatic system. We discuss how aging and injury-induced alterations disrupt mechanotransductive signaling compared to physiological conditions. Although candidate mechanosensors remain incompletely characterized, More >
Open Access
REVIEW
Leonardo Acuña1, Mariam Ahumada Sabagh2, Víctor David Osorio Castillo1,2, Caverly Gooden3, María Luisa Veisaga4, Juan Liuzzi5,6, Manuel A. Barbieri2,3,5,6,7,*
BIOCELL, DOI:10.32604/biocell.2026.079670
（This article belongs to the Special Issue: Bioactive Natural Components as Regulators of Cellular Pathways and Disease Progression)
Abstract Costunolide, a sesquiterpene lactone from Saussurea lappa Clarke, exhibits broad pharmacological properties, including anti-inflammatory and anticancer effects. This review examines its emerging potential as a host-directed antiviral compound. Costunolide modulates conserved host signaling pathways frequently exploited during viral infection, including nuclear factor-kappa B (NF-κB), the NOD-like receptor family pyrin domain-containing 3 (NLRP3) inflammasome, and mitogen-activated protein kinase (MAPK) cascades. Inhibition of NF-κB may suppress viral transcription in human immunodeficiency virus (HIV-1) infection, while NLRP3 blockade may limit inflammasome-driven viral reactivation in Epstein–Barr virus (EBV) infection and attenuate hyperinflammation in severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) More >
Open Access
REVIEW
Bianca Voicu Balasea1, Alexandra Popa2,*, Florentina Rus2, Radu Radulescu2, Melis Izet1, Alexandra Ripszky1,2,*
BIOCELL, DOI:10.32604/biocell.2026.082448
Abstract Oral squamous cell carcinoma (OSCC) is an aggressive malignancy often diagnosed at advanced stages and associated with poor prognosis. This review aims to summarize the role of Kirsten rat sarcoma viral oncogene homolog (KRAS) signaling in OSCC progression, with particular emphasis on its involvement in the regulation of autophagy, apoptosis, and oxidative stress. KRAS contributes to tumor progression despite the low frequency of activating mutations, primarily through increased KRAS expression associated with activation of downstream signaling pathways, including phosphoinositide 3-kinase/protein kinase B/mechanistic target of rapamycin (PI3K/AKT/mTOR) and rapidly accelerated fibrosarcoma/mitogen-activated protein kinase kinase/extracellular signal-regulated kinase More >
Open Access
REVIEW
Lichun Zhong1,#, Dijia Wu2,#, Sirui Zhang2, Wenjing Liu2, Faping Wang3,*, Fengming Luo3,*
BIOCELL, DOI:10.32604/biocell.2026.078898
（This article belongs to the Special Issue: Autophagy and Oxidative Stress in Cancer: Molecular Crossroads and Cell Fate Decisions)
Abstract Idiopathic pulmonary fibrosis (IPF) is an age-associated, progressive fibrotic interstitial lung disease with limited disease-modifying therapies and poor long-term outcomes. Increasing evidence indicates that senescence of alveolar type II epithelial (AT2) cells is not merely a bystander phenomenon but a central driver of epithelial dysfunction, failed alveolar regeneration, and fibrotic remodeling. In this narrative review, we summarize recent mechanistic, single-cell, epigenetic, and translational studies that have reshaped the epithelial-centered model of IPF. We first outline normal AT2 biology and the regenerative AT2-to-AT1 trajectory, and then discuss how telomere dysfunction, endoplasmic reticulum stress, mitochondrial injury, DNA More >
Open Access
REVIEW
Davide Nilo1,*, Giovanni di Lorenzo1, Marco La Montagna1, Riccardo Nevola2, Aldo Marrone1, Ferdinando Carlo Sasso1, Alfredo Caturano3
BIOCELL, DOI:10.32604/biocell.2026.081324
（This article belongs to the Special Issue: Cellular and Molecular Mechanisms of Gut Microbiota, Oxidative Stress, and Inflammation in Health and Disease)
Abstract Metabolically–dysfunction–associated steatotic liver disease (MASLD) is the most prevalent chronic liver disease worldwide and is increasingly recognized as a systemic disorder at the intersection of metabolic dysregulation, inflammation, and carcinogenesis. Progression from simple steatosis to metabolic dysfunction–associated steatohepatitis (MASH), fibrosis, and hepatocellular carcinoma (HCC) reflects the interplay between metabolic overload, oxidative stress, immune activation, and gut microbiota dysbiosis. In this review, we propose the Redox–Microbiota–Inflammatory Axis as an integrative framework linking metabolic stress to fibrogenesis and hepatocarcinogenesis. Nutrient excess and insulin resistance promote mitochondrial dysfunction and reactive oxygen species (ROS) generation, which activate redox-sensitive inflammatory More >
Open Access
REVIEW
Michele Manganelli*
BIOCELL, DOI:10.32604/biocell.2026.081268
Abstract Telomere homeostasis is intrinsically integrated into the cellular metabolic network through a complex mito-nuclear communication system. Telomeric chromatin acts as a sensitive sensor of mitochondrial flux, where the stability of telomeres depends on mitochondrial-derived metabolites essential for epigenetic remodeling. Three primary axes govern this control: (1) Acetyl-CoA-mediated histone acetylation necessary for human Telomerase Reverse Transcriptase (hTERT) expression; (2) the competitive balance between α-ketoglutarate/succinate, modulating Jumonji-C (JmjC)-demethylases and Ten-eleven translocation (TET) enzymes; (3) the mitochondrial NAD+/NADH ratio, governing sirtuin 6 (SIRT6) fidelity. The bidirectional non-coding RNA shuttling, TERC-53 fragment, acts as a retrograde signal of mitochondrial distress. More >
Open Access
MINI REVIEW
Amitabha Ray1,*, Thomas F. Moore2
BIOCELL, DOI:10.32604/biocell.2026.076530
Abstract Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2)-related critical illness, i.e., severe form of coronavirus disease 2019 (COVID-19), is associated with a hyperinflammatory state. In COVID-19 disease, several components of the body, including the complement system, different cells such as endothelial cells, platelets, monocytes, and neutrophils, and various pro-inflammatory cytokines such as interleukin-6 and tumor necrosis factor α, can contribute to a state of coagulopathy, and ultimately, all these factors cause extensive tissue damage. This pathological process may contribute to increased aggressiveness in cancer cells or to the reawakening of dormant cancer cells. Studies have documented More >
Graphic Abstract
Open Access
REVIEW
Jia-Feng Chang1,2, Ting-Yu Yeh3, I-Ta Lee4,*, Yue-Wen Chen5,6,*
BIOCELL, DOI:10.32604/biocell.2026.080855
（This article belongs to the Special Issue: Unraveling Periodontal Disease: Molecular and Cellular Perspectives)
Abstract Cardio-kidney-metabolic (CKM) syndrome and periodontal diseases are bi-directionally linked pathologies driven by systemic inflammation, oxidative stress, and metabolic dysregulation. Identifying pleiotropic therapeutic agents targeting this axis is a major clinical priority. This review evaluates the bio-cellular role of propolis, a natural resinous hive product, in mitigating CKM syndrome and periodontal disease. Propolis exerts robust protective effects by modulating key intracellular signaling pathways. Specifically, it upregulates nuclear factor erythroid 2-related factor 2 (Nrf2)-dependent antioxidant defenses, which subsequently interferes with redox-sensitive inflammatory triggers. Concurrently, it antagonizes pro-inflammatory signaling, including nuclear factor-kappa B (NF-κB), mitogen-activated protein kinase (MAPK), More >
Open Access
COMMENTARY
Malvina Hoxha1,*, Domenico Tricarico2, Loredana Capobianco3
BIOCELL, DOI:10.32604/biocell.2026.080846
（This article belongs to the Special Issue: Advances in Nrf2 Signaling Pathway in Neurodegenerative Diseases)
Abstract Arachidonic acid (AA) and its mediators, including prostaglandins (PGs) and lipoxygenase (LOX) products, have different and sometimes opposing effects on neuronal survival and inflammatory signaling. Evidence indicates a functional and dynamic interaction between AA-derived lipid mediators and the nuclear factor erythroid 2-related factor 2 (Nrf2), a master regulator of antioxidant and cytoprotective responses. Certain AA metabolites, such as the cyclopentenone prostaglandin 15-deoxy-Δ12,14-prostaglandin J2 (15d-PGJ2) and LOX-derived products including 5-oxo-eicosatetraenoic acid (5-oxo-ETE), have been shown to activate Nrf2 signaling. This activation enhances antioxidant defenses, promotes redox homeostasis, and mitigates inflammatory responses in neuronal and glial cells. In contrast, More >
Open Access
REVIEW
Irina Shalaginova*, Boris Bakulevskiy
BIOCELL, DOI:10.32604/biocell.2026.080400
（This article belongs to the Special Issue: Cellular and Molecular Mechanisms Underlying Complex Behaviors and Neuropsychiatric Disorders)
Abstract This review discusses the dual role of DNA double-strand breaks (DSBs) in the brain, where they can act as both physiological regulators of gene expression and contributors to neuronal dysfunction under pathological conditions. In post-mitotic neurons, which rely mainly on non-homologous end joining, the balance between DSB formation and repair appears to be especially important. Recent studies show that transient activity-induced DSBs, particularly at regulatory regions of immediate early genes (IEGs), support chromatin remodeling and transcriptional activation. In contrast, persistent DSBs associated with chronic stress, hyperexcitability, ageing, or neurodegenerative disorders are linked to impaired repair, More >
Open Access
MINI REVIEW
Antonio Montefusco1,*, Antonio Massimiliano Romanelli2, Ivana Caputo1, Gaetana Paolella1,*
BIOCELL, DOI:10.32604/biocell.2026.079770
（This article belongs to the Special Issue: Cellular Mechanisms and Delivery Strategies of Anticancer Agents: From Pharmacologically Active Molecules to Engineered Systems)
Abstract Cancer therapy is increasingly shifting towards targeted strategies capable of maximizing therapeutic efficacy while minimizing off-target toxicity. Extracellular vesicles (EVs), including exosomes and microvesicles, have emerged as promising natural nanocarriers due to their characteristics like biocompatibility, stability in biological fluids, and capacity for selective cargo delivery. EVs participate in intercellular communication through highly regulated biological processes that control their formation, cargo selection, cellular uptake, and downstream signaling activity. This mini-review highlights how regulated sorting processes, surface-associated tropism, and diverse internalization pathways determine EVs specificity and functional impact in recipient tumor cells. Furthermore, current advances in More >
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