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
ARTICLE
Katerina Basharova1,2,#,*, Anastasia Bezrukova1,2,#, Alena Kopytova1,2, Anna Lavrinova1,2, Galina Baydakova3, Irina Miliukhina1,4, Ekaterina Zakharova1,3, Anton Emelyanov1,2, Sofya Pchelina1,2, Tatiana Usenko1,2,*
BIOCELL, DOI:10.32604/biocell.2026.079585
（This article belongs to the Special Issue: Cellular and Molecular Mechanisms in Parkinson's Disease: Novel Targets and Biomarkers for Target Therapy)
Abstract Objectives: Synucleinopathies—Parkinson’s disease (PD), dementia with Lewy bodies (DLB), and multiple system atrophy (MSA)—involve alpha-synuclein aggregation and lysosomal dysfunction. We conducted a longitudinal study of lysosomal hydrolase activities and lysosphingolipid levels in blood and PBMC-derived macrophages from patients, and assessed the effects of LRRK2 inhibition (MLi-2). Methods: Blood and PBMC-derived macrophages were collected from patients with idiopathic PD (iPD), DLB, MSA, and controls. Enzyme activities (GCase, ASMase, GLA, GALC) and lysosphingolipids (HexSph, LysoGb3, LysoSM) were measured. Autophagy markers (p62, LC3B-II) and cathepsin D (CTSD) were analyzed by western blot. Effects of MLi-2 were evaluated in macrophages. Results:… 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
ARTICLE
Bin Lian1,2,#, Na You2,3,#, Jingyu Wang4, Cong Wang4, Yunjie Wen2, Jiandong Wang5,*
BIOCELL, DOI:10.32604/biocell.2026.081166
Abstract Background: Rho GTPase-activating protein 40 (ARHGAP40), downregulated in various tumors, including basal cell carcinoma, has an unclear role in colorectal cancer (CRC). This study aimed to elucidate the function and clinical significance of ARHGAP40 in CRC. Methods: ARHGAP40 expression in CRC tissues was evaluated by immunohistochemistry and analyzed in relation to clinicopathological features and patient survival. Gain- and loss-of-function experiments were performed in CRC cell lines to assess cell proliferation, apoptosis, migration, and invasion. RNA sequencing, co-immunoprecipitation, Ras homolog gene family member A (RhoA) activation assays, and rescue experiments were conducted to explore the underlying mechanism. Results:… 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
ARTICLE
Lea Barbarić1, Marina Oskomić1, Anđela Horvat2, Katja Ester2, Nikolina Stojanović3, Ana Tomašić Paić1, Mihaela Matovina1,*
BIOCELL, DOI:10.32604/biocell.2026.080282
Abstract Objectives: Dipeptidyl peptidase 3 (DPP3) is a zinc metallopeptidase involved in peptide turnover and possibly in blood pressure and pain regulation. It also modulates oxidative stress response via the Kelch-like ECH-associated protein 1–nuclear factor erythroid 2-related factor 2 (KEAP1–NRF2) pathway. Although frequently upregulated in cancer, its role in carcinogenesis remains unclear. This study examined the effects of DPP3 knockdown (KD) and overexpression on migration, proliferation, and KEAP1–NRF2 pathway regulation in HeLa cells. Methods: We assessed the effects of DPP3-KD and overexpression on HeLa cell migration using a wound healing assay, and on NRF2 activity by measuring… More >
Open Access
ARTICLE
Laura Schaltz1,2, Simon Lassnig1,2, Karola Schlote1,2, Christian Schwerk3, Horst Schroten3, Nicole de Buhr1,2,*
BIOCELL, DOI:10.32604/biocell.2026.079046
（This article belongs to the Special Issue: Neuroinflammation and Neuroprotection in CNS Diseases: From Mechanisms to Therapeutic Targets)
Abstract Objectives: Streptococcus suis (S. suis) is a worldwide occurring pathogen in pigs and humans that can cross the blood-cerebrospinal fluid barrier (BCSFB) to cause meningitis, while host neutrophils counter infection through mechanisms including the release of neutrophil extracellular traps (NETs). NET-formation involves the release of nuclear DNA with antimicrobial components, which can bind and kill bacteria. We aimed to characterize the host-pathogen interaction between S. suis and neutrophils within the CSF compartment, focusing on NET-formation. Methods: A 3D cell culture model of the porcine BCSFB was used by cultivating a porcine choroid plexus epithelial cell line (PCP-R) on filter… More >
Open Access
ARTICLE
Zebiao Liu1,#, Xuebing Zhan1,#, Mingquan Chen1, Junxi Lai2, Wenli Zhao1,*
BIOCELL, DOI:10.32604/biocell.2026.081173
Abstract Background: Immunosuppression contributes to breast cancer treatment failure, yet Cluster of Differentiation 74 (CD74) function in macrophages remains unclear. This study investigated how CD74 influences M1 macrophage polarization and its functional and expression profiles in breast cancer. Methods: We used bioinformatics analysis combined with in vitro cell experiments. The expression of CD74 in THP-1-derived M1 macrophages induced by Lipopolysaccharide/Interferon-gamma (LPS/IFN-γ) was knocked down by shRNA. Polarization markers were detected by WB, qPCR, and flow cytometry. Cytokines were detected by Enzyme-Linked Immunosorbent Assay (ELISA). The phagocytosis and killing effect of macrophages on MCF-7 cells were evaluated by a… More >
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
REVIEW
Mohammad Muzaffar Mir1,*, Rashid Mir2,3, Badr A. Alsayed4, Mohammed M. Jalal3, Malik A. Altayar3, Hanan M. Aljammaz5, Zinab Alatawi6, Khalid A. Alfifi2, Basmah M. Alenzi7, Mohammad Tanveer Khaji8, Umair Ismail9, Ghada Mohamed10,11, Nada Zai Sageer12, Abdullatif Taha Babakr13, Saba M. Mir14, Ulfat Jan15
BIOCELL, DOI:10.32604/biocell.2026.077540
Abstract The tuberculosis (TB) epidemic continues to be one of the largest public health challenges affecting people globally, especially due to late diagnosis, disease monitoring, and prognosis. Currently used diagnostic tools have variable sensitivity and accessibility, and many have limited ability to differentiate between latent and active TB. In case of TB, exosomes from cells infected with Mycobacterium tuberculosis (M. tuberculosis) have disease-specific antigens, microRNAs, and other molecular components, which make them potential diagnostic and prognostic biomarkers. This review focuses on previously published literature regarding the role of exosomes and exosomal antigens in TB screening and prognostication. It… More >
Open Access
REVIEW
Babu Santha Aswani1,#, Bethsebie Lalduhsaki Sailo1,#, Young Yun Jung2,#, Sosmitha Girisa1, Mangala Hegde1, Mohammed S Alqahtani3,4, Mohamed Abbas5, Hassan Ali Almubarak6, Anupam Bishayee7, Kwang Seok Ahn2,*, Ajaikumar B. Kunnumakkara1,*
BIOCELL, DOI:10.32604/biocell.2026.073397
（This article belongs to the Special Issue: Natural Product-Based Anticancer Drug Discovery)
Abstract Despite the advancements achieved in chemotherapy, cancer continues to remain a formidable and lethal global threat, ranking as the second leading cause of death worldwide. The development of chemoresistance poses a significant hurdle in cancer treatment. Nonetheless, a therapeutic strategy known as chemosensitization has emerged to counteract cancer cell resistance, wherein the efficacy of one drug is augmented by another. Accumulating evidence suggests that natural products have attracted considerable attention in the cancer therapeutic realm due to their ability to combat multidrug resistance with minimal side effects. Ginsenosides, triterpene saponins extracted from Panax ginseng, have demonstrated… More >
Graphic Abstract
Open Access
REVIEW
Dominick Shoha#, David Lei#, Tyler Truong, Sophia Strukel, Elliot Enshaie, Vikrant Rai*
BIOCELL, DOI:10.32604/biocell.2026.078846
（This article belongs to the Special Issue: Unraveling the Interplay of Molecular and Cellular Mechanisms between Diabetes and Non-communicable Diseases )
Abstract Diabetes, inflammation, and neurodegeneration, particularly Alzheimer’s disease (AD), are deeply interconnected (brain diabetes). Type 2 diabetes mellitus (T2DM) acts as a significant risk factor for neurodegenerative diseases like Alzheimer’s (AD) and Parkinson’s (PD) by inducing chronic inflammation, oxidative stress, and metabolic dysfunction. Hyperglycemia drives neuroinflammation and damages the blood-brain barrier (BBB), exacerbating cognitive decline and neuronal loss. Chronic inflammation acts as a central bridge, linking high blood sugar, insulin resistance, and metabolic dysfunction in the brain to the buildup of amyloid plaques, tau tangles, and neuronal damage due to shared insulin signaling issues in the 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 >
Open Access
REVIEW
Mihaela Jurdana1,*, Lovro Ziberna2,3
BIOCELL, DOI:10.32604/biocell.2026.079591
Abstract Obesity and metabolic syndrome promote malignancies through chronic inflammation and sustained activation of insulin and insulin-like growth factor-1 (IGF-1) signaling. Skeletal muscle is central to this tumor-promoting milieu because it governs insulin-stimulated glucose disposal, lipid oxidation, and endocrine crosstalk. This narrative review explores whether melatonin signaling in skeletal muscle, particularly via melatonin receptor 2 (MT2), represents a modifiable node within the obesity–cancer axis. Experimental evidence indicates that melatonin activates MT2-linked Gi/o and calcium-sensitive pathways converging on phosphoinositide 3-kinase–protein kinase B (PI3K–Akt), extracellular signal-regulated kinases (ERK), and calcium/calmodulin-dependent protein kinase II–adenosine monophosphate-activated protein kinase–peroxisome proliferator-activated receptor gamma More >
Open Access
REVIEW
Yibing Wang1, Xingbo Wu1, Yifei Shen1, Xiayi Wang1, Chun Hung Chu2, Irene Shuping Zhao2,3, Xueqi Gan1,*
BIOCELL, DOI:10.32604/biocell.2026.079089
（This article belongs to the Special Issue: Modulation of Inflammation, Oxidative Stress, and Mitochondrial Function: Therapeutic Perspectives Across Diseases)
Abstract Periodontitis is a prevalent inflammatory disease characterized by the progressive destruction of tooth-supporting tissues. Its pathogenesis remains incompletely understood, but accumulating evidence highlights mitochondrial dynamics imbalance and oxidative stress as interconnected drivers. However, comprehensive reviews elucidating the molecular basis of this interaction are lacking. Therefore, this review aims to clarify the crosstalk between mitochondrial dynamics dysregulation and oxidative stress, and how this bidirectional interaction contributes to periodontal tissue destruction. This review first provides an overview of mitochondrial dynamics and the mechanisms of oxidative stress. We then contextualize these processes within periodontitis, detailing the dual role More >
Open Access
REVIEW
Deborah Joyce1, Wan Muhammad Farhan Syafiq Wan Mohd Nor2, Ivy Chung2, Amira Hajirah Abd Jamil1, Nur Akmarina Mohd Said1,*
BIOCELL, DOI:10.32604/biocell.2026.077378
Abstract Non-coding RNAs (ncRNAs) and cholesterol metabolism have independently been recognized as critical regulators of cancer progression. NcRNAs modulate various aspects of cancer cell behaviour, including metabolic reprogramming, proliferation, migration, and intercellular communication. Concurrently, dysregulated cholesterol metabolism has emerged as a hallmark of cancer, influencing tumour growth, immune evasion, chemoresistance, and metastasis. While numerous studies have explored the role of ncRNAs like long non-coding RNAs (lncRNAs) and circular RNAs (circRNAs) in modulating cholesterol metabolism within either cancer cells or immune cells, the mechanism of their action largely depends on the involvement of microRNAs (miRNAs). However, the… More >
Open Access
REVIEW
Zhiqing Hu1, Lisha Ma2, Weili Zhu2,*
BIOCELL, DOI:10.32604/biocell.2026.077860
（This article belongs to the Special Issue: Novel Targeted Therapy in Oncology)
Abstract Ovarian cancer (OC) is the most lethal gynecologic malignancy. The current first-line treatment still relies primarily on cisplatin-based chemotherapy, yet cisplatin resistance strongly predicts poor patient prognosis. Cuproptosis is a newly identified cell death modality driven by copper overload and impaired mitochondrial respiration. This review outlines the core molecular mechanisms of cuproptosis and examines its complex association with cisplatin resistance in ovarian cancer. Their interplay involves shared transport systems. In cisplatin-resistant ovarian cancer cells, copper influx transporter Copper Transporter 1 (CTR1) downregulation and efflux transporter ATPase copper transporting alpha/beta polypeptide (ATP7A/B) upregulation reduce the intracellular… More >
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