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  • Open Access

    MINI REVIEW

    The Impact of COVID-19 on Breast Cancer and the Role of Neutrophil Extracellular Traps

    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

    The Impact of COVID-19 on Breast Cancer and the Role of Neutrophil Extracellular Traps

  • Open Access

    ARTICLE

    Dipeptidyl Peptidase 3 Knockdown in HeLa Cells Induces G0/G1 Cell Cycle Arrest Associated with Upregulation of p21 Protein

    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

    Characterization of Alive and Impaired NET-Releasing Neutrophils in A Model of the Blood-Cerebrospinal Fluid Barrier after Streptococcus suis Infection

    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

    CD74 Drives M1 Macrophage Polarization via STAT3 Signaling to Promote Antitumor Immunity in Breast Cancer

    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

    From Cardio-Kidney-Metabolic Syndrome to Periodontal Diseases: The Bio-Cellular Role of Propolis

    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

    ARTICLE

    Mitochondrial Calcium Uniporter (MCU) Inhibition Disrupts Bone Remodeling and Impairs Mitochondrial Function via Aberrant Mitochondrial Dynamics

    Xinliang Fu1,#, Wen Du1,#, Tao Li2, Yifei Shen1, Ngai-Fung Ruan1, Huiling Ling1, Xingbo Wu1, Ziqi Qin1, Xiting Zhu1, Xueqi Gan1,*
    BIOCELL, DOI:10.32604/biocell.2026.077349
    (This article belongs to the Special Issue: MitoROS: Exploring Mitochondria and Oxidative Stress)
    Abstract Objectives: Mitochondrial function is intricately linked to osteogenic and osteoclastic differentiation. The mitochondrial calcium uniporter (MCU) is a critical regulator of mitochondrial function, influencing key aspects of cellular metabolism and signaling. However, the precise mechanisms by which MCU modulates osteogenic activity remain unclear. This study aimed to elucidate the impact of MCU-mediated regulation of mitochondrial function on bone remodeling and to explore the underlying mechanisms. Methods: The mouse pre-osteoblastic cells (MC3T3-E1) were treated with the MCU-specific inhibitor Ru265 during osteogenic induction to assess changes in osteogenic differentiation capacity, mitochondrial function, and mitochondrial dynamics. Additionally, MCU global… More >

  • Open Access

    COMMENTARY

    Arachidonic Acid Mediators and Nrf2 in Neurodegenerative Diseases

    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

    Physiological and Pathological DNA Double-Strand Breaks in the Central Nervous System

    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

    Emerging Roles of Exosomes and Exosomal Antigens as Potential Diagnostic and Prognostic Agents for Mycobacterium tuberculosis Infection

    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

    Improving Cancer Therapy: The Strong Synergy of Ginsenosides and Chemotherapy

    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

    Improving Cancer Therapy: The Strong Synergy of Ginsenosides and Chemotherapy

  • Open Access

    REVIEW

    Interaction of Cellular and Molecular Mechanisms in Diabetes-Associated Neurodegeneration and Alzheimer’s Disease

    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

    ARTICLE

    Organ-Specific Metabolic Adaptations to Acute Injury and Their Modulation by Fumarate

    Marina I. Buyan1,2,#, Kseniia S. Cherkesova1,3,#, Anna A. Brezgunova1, Andrey I. Buyan4, Polina A. Abramicheva1, Irina B. Pevzner1, Nadezda V. Andrianova1,*, Egor Y. Plotnikov1,*
    BIOCELL, DOI:10.32604/biocell.2026.078925
    Abstract Objectives: Metabolic substrate deficiency is a key factor in many pathologies, with organ vulnerability depending on specialized metabolic profiles. In this study, we aimed to investigate the impact of deprivation stress on mitochondria and cell functions in different cell types and to assess the potential of fumarate, a tricarboxylic acid (TCA) cycle intermediate, to modulate these stress responses. Methods: We assessed the effects of fumarate on cell proliferation and mitochondrial membrane potential under both normal conditions and serum deprivation in vitro in astrocytes, renal epithelial cells, and hepatic stellate cells. Subsequently, we performed bioinformatic analysis of transcriptomic… More >

  • Open Access

    ARTICLE

    Modulating the Biological Processes and Glycolysis of Hepatocellular Carcinoma Cells by UBR7’s Suppression of Pyruvate Kinase PKM2

    Bo Liu, Xue Li*
    BIOCELL, DOI:10.32604/biocell.2026.077797
    Abstract Background: As a key glycolytic enzyme, Pyruvate kinase M2 (PKM2), which is highly expressed in cancer cells, promotes hepatocellular carcinoma (HCC) proliferation/metastasis. This research investigates the involvement of Ubiquitin protein ligase E3 component N-recognin 7 (UBR7) in HCC progression/glycolysis and its potential mechanisms. Methods: UBR7 expressions in HHL-5, Huh-7, and HepG2 cells were investigated using Quantitative Reverse Transcription Polymerase Chain Reaction and Western Blot. Cell counting kit-8, clone formation experiment, scratch-wound assay, and transwell testing were conducted to assess the malignant biological behaviors of HepG2 and Huh-7 cells; the absorption level of glucose and generation levels… More >

  • Open Access

    ARTICLE

    Linalool Promotes Osteoblast Differentiation via SELENBP1-Dependent Signaling in MC3T3-E1 and C3H10T1/2 Cells

    Kyeong-Min Kim1,2, A-Rang Kim1,2, Won-Gu Jang1,2,3,*
    BIOCELL, DOI:10.32604/biocell.2026.077163
    (This article belongs to the Special Issue: Innovations in Musculoskeletal Biology, Disease, and Regeneration)
    Abstract Background: Linalool is a monoterpene alcohol with known anti-inflammatory and antioxidant properties, but its role in osteoblast differentiation remains unclear. This study aimed to investigate the osteogenic potential of linalool and to examine the role of selenium-binding protein 1 (Selenbp1) in mediating its effects. Methods: Murine MC3T3-E1 and C3H10T1/2 cells were treated with linalool under osteogenic conditions. Osteoblast differentiation was assessed by alkaline phosphatase (ALP) activity, Alizarin Red S staining, and expression of runt-related transcription factor 2 (Runx2) and distal-less homeobox 5 (Dlx5). The involvement of Selenbp1 was examined using siRNA knockdown and plasmid overexpression. A… More >

  • Open Access

    ARTICLE

    METTL3-Mediated m6A Regulation of PTEN Promotes Macrophage Ferroptosis in Gouty Arthritis

    Gang Yang#, Xiongwu Long#, Xingchang Fu*
    BIOCELL, DOI:10.32604/biocell.2026.075362
    (This article belongs to the Special Issue: Targeting Inflammatory Diseases with Novel Strategies: Cellular and Molecular Mechanisms)
    Abstract Objectives: Macrophage ferroptosis is linked to the pathogenesis of gouty arthritis (GA), yet the precise regulatory mechanism needs to be elucidated. This study aimed to investigate the role of macrophage ferroptosis in GA and its potential mechanisms. Methods: THP-1 macrophages were stimulated with monosodium urate (MSU) crystals to simulate the GA model. The co-culture system of macrophages and primary chondrocytes (hCDs) was employed to analyze the effects of macrophage-mediated inflammation on chondrocyte degeneration. Results: MSU stimulation induced ferroptosis in macrophages, accompanied by increased methyltransferase-like 3 (METTL3) expression (p = 0.003) and total m6A modification level (p = 0.0058).… More >

  • Open Access

    REVIEW

    Decoding Enterovirus 71: Molecular Functions of Structural and Nonstructural Proteins in Viral Replication and Host Manipulation

    Jiamei Wu1,*, Yuechuan Zhang2, Junxue Wu2, Chengxin Hao1
    BIOCELL, DOI:10.32604/biocell.2026.071704
    Abstract Enterovirus 71 (EV71), a member of the family Picornaviridae, genus Enterovirus, is an agent of hand, foot, and mouth disease (HFMD) and remains a persistent global health concern, particularly among children under five years of age. Although most infections are self-limiting, a significant proportion can progress to severe neurological manifestations such as aseptic meningitis, encephalitis, and fatal pulmonary oedema. Despite substantial advances in research, no universally effective antiviral therapy or broadly protective vaccine has yet been developed. Drawing upon both foundational and recent studies, we evaluate the strength of existing evidence and delineate how these viral… More >

  • Open Access

    MINI REVIEW

    Extracellular Vesicles as Promising Carriers in Cancer Therapy: Molecular Mechanisms of Biogenesis, Targeting, and Intracellular Action

    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

    Targeting Skeletal Muscle Melatonin-MT2 Signaling to Attenuate the Obesity-Cancer Axis: A Metabolic Perspective

    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

    Mitochondrial Dynamics and Oxidative Stress in Periodontitis

    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

    ARTICLE

    Overexpression of GluN2B Regulates Neuroinflammation through the BDNF/TrkB Signaling Pathway to Improve Postoperative Cognitive Dysfunction

    Bohan Lin#, Wei Liu#, Xiu Ni, Fuyi Shen*
    BIOCELL, DOI:10.32604/biocell.2026.077413
    Abstract Background: Postoperative cognitive dysfunction (POCD) is a common neurological complication in elderly patients. However, the mechanism by which glutamate ionotropic receptor NMDA type subunit 2B (GluN2B) contributes to POCD development remains incompletely understood. This study aimed to investigate the effects of GluN2B overexpression on POCD improvement and elucidate its underlying molecular mechanisms. Methods: In vitro, lipopolysaccharide (LPS) was used to induce inflammation in mouse primary microglia, and a microglia-HT22 neuron co-culture system was established to simulate the neurotoxic environment. Overexpression and knockdown constructs for GluN2B and brain-derived neurotrophic factor (BDNF) were generated. Western blot, ELISA, immunofluorescence, and… More >

  • Open Access

    REVIEW

    Cholesterol-Mediated Remodelling of the Tumour-Immune Landscape: The Role of Non-Coding RNAs

    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

    ARTICLE

    miR-216a-5p Improves Macrophage M1 Polarization and Pyroptosis in URSA via Modulating HMGB1 to Regulate TLR4/NF-κB/NLRP3 Axis

    Weina Xu1, Yi Xia1, Qing Shen1, Ling Ai1, Yingye Lu2,*
    BIOCELL, DOI:10.32604/biocell.2026.076001
    Abstract Background: Dysfunction of decidual macrophages (dMφ) mediated by high mobility group box 1 (HMGB1) is related to unexplained recurrent spontaneous abortion (URSA), but its upstream regulatory mechanism remains unclear. The research explores whether miR-216a-5p regulates the toll-like receptor 4/nuclear factor-κB/nucleotide-binding oligomerization domain-like receptor protein 3 (TLR4/NF-κB/NLRP3) signaling axis by targeting HMGB1, thereby affecting the M1 polarization and pyroptosis of dMφ in URSA. Methods: The URSA mouse model was established, and primary dMφ was isolated and cultured. HMGB1 and miR-216a-5p were overexpressed or knocked down. Their expressions were examined. Their targeting relationship was verified through a bioinformatics… More >
    Graphic Abstract

    miR-216a-5p Improves Macrophage M1 Polarization and Pyroptosis in URSA via Modulating HMGB1 to Regulate TLR4/NF-κB/NLRP3 Axis

  • Open Access

    ARTICLE

    12-O-Tetradecanoylphorbol-13-Acetate Inhibits TGF-β1-Induced Proliferation and Fibrosis in LX-2 Hepatic Stellate Cells by Regulating both YAP and AKT Activities

    Moo Hyun Kim1, Yongdae Yoon2, Chang Wan Kim1, Jun-Won Lee3, Bhupendra Regmi2, Saher Fatima2, Moon Young Kim2,3, Soon Koo Baik2,3, Pil Young Jung1,*, Young Woo Eom2,*
    BIOCELL, DOI:10.32604/biocell.2026.076364
    Abstract Background: Although transforming growth factor-β (TGF-β) drives hepatic stellate cell activation and fibrogenesis, the mechanisms by which 12-O-tetradecanoylphorbol-13-acetate (TPA) modulates these processes in TGF-β1-activated hepatic stellate cells remain to be determined. Therefore, we investigated whether TPA alleviates fibrosis in TGF-β1-treated hepatic stellate cells and regulates both canonical and non-canonical pathways. Further, we assessed whether inhibitors of these pathways similarly affect proliferation and fibrosis in LX-2 cells. Methods: LX-2 hepatic stellate cells were used as the experimental model. Cells were treated with TPA, TGF-β, or TGF-β plus TPA, and Yes-associated protein (YAP) and protein kinase B (PKB;… More >

  • Open Access

    REVIEW

    Research Progress on Cuproptosis in Cisplatin-Resistant Ovarian Cancer

    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 >

  • Open Access

    REVIEW

    Gut Microbiota-Derived Exosomes Are Unique Natural Nanocarriers for Therapeutics

    Ibrahim M. Ibrahim1, Shadab Md2,*
    BIOCELL, DOI:10.32604/biocell.2026.077548
    (This article belongs to the Special Issue: Bioactive Natural Components as Regulators of Cellular Pathways and Disease Progression)
    Abstract Gut microbiota-derived exosomes (MDEs) have emerged as a novel class of drug delivery and are secreted by bacteria, fungi, and archaea in the human microbiota within the human intestinal ecosystem and possess inherent biocompatibility and lower immunogenicity, enabling seamless integration within host intestinal and systemic bioenvironments. This review elucidates the cellular and molecular mechanisms governing MDE function, explaining how their unique lipid bilayer composition facilitates cellular entry via receptor-mediated endocytosis and membrane fusion. This review discusses how gut MDEs traverse biological barriers, such as the blood-brain barrier and intestinal mucosa, by modulating tight junction proteins… More >
    Graphic Abstract

    Gut Microbiota-Derived Exosomes Are Unique Natural Nanocarriers for Therapeutics

  • Open Access

    ARTICLE

    Knockdown of PKM2 Promotes Proliferation and Neuronal Differentiation of Neural Stem Cells by Inhibiting PINK1/Parkin-Mediated Excessive Mitophagy

    Junming Yan, Boran Xiong, Yingjie Zhu*
    BIOCELL, DOI:10.32604/biocell.2026.075319
    (This article belongs to the Special Issue: Homeostasis of Mitochondria: Unraveling its Multifaceted Role in Health and Disease)
    Abstract Objective: Neural stem cells (NSCs) are essential for replenishing nerve cells, providing neuroprotection, and repairing damaged brain function, while mitophagy is critical for maintaining NSCs’ homeostasis. The study investigated whether pyruvate kinase M2 (PKM2) regulates NSCs’ proliferation and differentiation by modulating mitophagy. Method: This study established a model of excessive autophagy in neural stem cell mitochondria induced by cobalt chloride (CoCl2) and used plasmid transfection technology to knock down PKM2 expression, examining its effects on NSCs proliferation and differentiation. Additionally, potential mechanisms were explored by overexpressing phosphatase and tensin homolog-induced putative kinase 1 (PINK1) and adding the… More >
    Graphic Abstract

    Knockdown of PKM2 Promotes Proliferation and Neuronal Differentiation of Neural Stem Cells by Inhibiting PINK1/Parkin-Mediated Excessive Mitophagy

  • Open Access

    ARTICLE

    Lycium Barbarum Polysaccharides Upregulate Trx2 in Schwann Cells through ESR1 to Repair Sciatic Nerve Injury in Rats

    Guoxu Ma, Yonglu Huang, Fan Gong, Jianke Wu, Yi Ding, Ziyang Zhang, Xiaoliang Li, Jian Gao, Tingting Dang, Bowen Zhang*
    BIOCELL, DOI:10.32604/biocell.2026.078402
    (This article belongs to the Special Issue: Bioactive Natural Components as Regulators of Cellular Pathways and Disease Progression)
    Abstract Objectives: Sciatic nerve injury (SNI) impairs quality of life, and Lycium barbarum polysaccharides (LBP) may exert therapeutic effects via regulating Schwann cell (SC) mitochondrial stability, though the mechanism remains unclear. The study aimed to elucidate the therapeutic mechanisms of LBP in mitigating sciatic nerve injury by protecting Schwann cells via the estrogen receptor 1 (ESR1)/thioredoxin 2 (Trx2) pathway. Methods: An in vitro SNI model was established by inducing RSC96 cells with H2O2. Cell counting kit-8 (CCK8) assay, enzyme-linked immunosorbent assay (ELISA), Western blot, reactive oxygen species (ROS) and adenosine triphosphate (ATP) quantification, and mitochondrial membrane potential (MMP) detection were… More >

  • Open Access

    REVIEW

    Cellular Senescence in the Cardiovascular System: Molecular Mechanisms, Pathophysiology, and Senotherapeutic Interventions

    Beata Franczyk1, Anna Bajer1,#, Anna Bulicz1,#, Mikołaj Grabarczyk1,#, Paulina Jakubowska1,#, Katarzyna Krawiranda1,#, Natalia Kustosik1,#, Przemysław Kuzar1,#, Klaudia Leszto1,#, Maja Mejza1,#, Weronika Mstowska1,#, Jacek Rysz2, Ewelina Młynarska1,*
    BIOCELL, DOI:10.32604/biocell.2026.075767
    (This article belongs to the Special Issue: Cellular Senescence in Health and Disease)
    Abstract Cellular senescence and the Senescence-Associated Secretory Phenotype (SASP) play both physiological and pathological roles in the cardiovascular system. While transient senescence aids regeneration, chronic accumulation of senescent cells promotes endothelial dysfunction, arterial stiffening, and maladaptive cardiac remodeling. This review elucidates the pivotal role of the immune system in senescent cell clearance and explores how immunosenescence drives systemic low-grade inflammation. Significant emphasis is placed on emerging pharmacological strategies, specifically senolytics and senomorphics, assessing their capacity to restore cardiac function and attenuate atherosclerosis. Additionally, the utility of molecular biomarkers and diverse in vitro and in vivo models is analyzed More >

  • Open Access

    REVIEW

    Neuroinflammation and Oxidative Stress: Their Pathophysiological Roles in Amyotrophic Lateral Sclerosis and Alzheimer’s Disease

    Aslı Aykaç1,*, Eda Becer2, Ahmet Özer Şehirli3
    BIOCELL, DOI:10.32604/biocell.2026.077114
    (This article belongs to the Special Issue: Cellular and Molecular Mechanisms of Neurodegeneration: From Pathogenesis to Therapeutic Strategies)
    Abstract Neurodegenerative diseases such as Amyotrophic Lateral Sclerosis (ALS) and Alzheimer’s disease (AD) are driven by complex, multifactorial mechanisms in which oxidative stress (OS) and neuroinflammation (NI) play central, mutually reinforcing roles. Their interaction is mediated through key signaling pathways, including nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB), nuclear factor erythroid 2–related factor 2–Kelch-like ECH-associated protein 1 (Nrf2-Keap1), and the mitogen-activated protein kinase (MAPK) pathway, as well as mitochondrial dysfunction, microglial activation, and dysregulated redox homeostasis. Increasing attention has been directed toward understanding how Food and Drug Administration (FDA)-approved neuroprotective agents influence these interconnected processes. More >

  • Open Access

    REVIEW

    Extracellular Vesicles in Acute Myeloid Leukemia: Biology, Diagnostic Applications, and Therapeutic Potential

    Rashid Mir1,*, Jameel Barnawi1, Naseh A. Algehainy1, Mohammed M. Jalal1, Malik A. Altayar1, Mohammad A. Alanazi1, Mamdoh Moawadh1, Faris J. Tayeb1, Syed Khalid Mustafa2, Abdullatif Taha Babakr3, Umair Manghrio4, Jaber Alfaifi5, Faisal H. Altemani1
    BIOCELL, DOI:10.32604/biocell.2026.076199
    (This article belongs to the Special Issue: Epigenetic and ncRNA Biomarkers in Cancer: Diagnostic and Prognostic Value)
    Abstract Acute Myeloid Leukemia (AML) is one of the most complex hematological malignancies associated with the rapid production of immature myeloid cells and poor prognosis, even with the development of therapeutic options. Exosomes, which are extracellular vesicles with sizes ranging from 30 to 150 nm, have drawn a lot of interest because of their capacity to carry molecular cargoes, including DNA, mRNA, and non-coding RNAs. Various cells produce these vesicles, which have been shown to effectively transport their molecular contents to target cells via a variety of bodily fluids. This review comprehensively discusses the importance of More >

  • Open Access

    REVIEW

    Polyphenols in mtDNA Repair, Mitochondrial Biogenesis, and Mitophagy: An Integrative Review

    Desirée Victoria-Montesinos*, Pablo Barcina-Pérez*, Ana María García-Muñoz
    BIOCELL, DOI:10.32604/biocell.2026.077286
    (This article belongs to the Special Issue: MitoROS: Exploring Mitochondria and Oxidative Stress)
    Abstract Mitochondrial dysfunction is a central hallmark of metabolic, hepatic, cardiovascular, and neurodegenerative diseases. Dietary polyphenols modulate mitochondrial pathways, but their integrated effects remain poorly appreciated. This narrative review synthesizes preclinical and clinical evidence on four polyphenols (resveratrol, epigallocatechin-3-gallate, quercetin, and oleuropein) and examines their mechanisms in mitochondrial biogenesis, mtDNA protection, and mitophagy. Experimental studies indicate that these compounds activate conserved adaptive pathways, including sirtuin 1 (SIRT1) and peroxisome proliferator-activated receptor gamma coactivator 1 alpha (PGC-1α), AMP-activated protein kinase (AMPK), and PTEN-induced kinase 1 (PINK1) with Parkin, therapy enhancing mitochondrial biogenesis, reducing oxidative stress, and promoting More >

  • Open Access

    REVIEW

    Restoring Homeodynamics: Autophagy, Ageing and the Metabolic Correction of Disease

    Andrew Scarborough1, Yvoni Kyriakidou1, Derek C. Lee2, Tomás Duraj2, Thomas N. Seyfried2, Isabella D. Cooper1,*
    BIOCELL, DOI:10.32604/biocell.2026.074152
    (This article belongs to the Special Issue: Homeostasis of Mitochondria: Unraveling its Multifaceted Role in Health and Disease)
    Abstract The global rise in chronic, non-communicable diseases (NCDs) is inextricably linked to metabolic dysfunction, with hyperinsulinaemia acting as a potent upstream driver of ageing and age-related disease. Some of the most burdensome diseases of our time, including type 2 diabetes, cardiovascular disease, cancer, and neurodegenerative conditions, such as Alzheimer’s disease (AD), are largely underpinned by insulin resistance as part of a broader system of metabolic and mitochondrial dysfunction. These pathologies are particularly pronounced in the developed world, where obesity and other lifestyle-related conditions are major contributors to disease burden and premature mortality. As an upstream… More >

  • Open Access

    REVIEW

    Revisiting Vesicle Trafficking in Astrocytes

    Jernej Jorgačevski1,2, Maja Potokar1,2,*
    BIOCELL, DOI:10.32604/biocell.2026.077871
    (This article belongs to the Special Issue: Transporters and Channels in Brain Physiology: From Molecular Biophysics to Cellular Dynamics)
    Abstract Astrocytes contribute to central nervous system (CNS) homeostasis by taking up and releasing various transmitters, ions, water, and energy molecules, thereby modulating neuronal function and maintaining the blood-brain barrier. The dynamic delivery, retrieval, and recycling of transporters, channels, receptors, and vesicular cargo at the astrocyte plasma membrane are regulated by the cytoskeleton networks composed of microtubules, actin filaments, and intermediate filaments. Increasing evidence indicates that changes in vesicle trafficking disrupt astrocyte–neuron communication and contribute to CNS dysfunction in pathological conditions. This review presents recent findings on vesicle trafficking in astrocytes with emphasis on the cytoskeletal More >

  • Open Access

    REVIEW

    Mitochondria as the Bridge between Injury and Protection: The Role of Melatonin in Non-Steroidal Anti-Inflammatory Drug-Induced Gastric Ulcers

    Debasish Bandyopadhyay1,*, Romit Majumder1,2,#, Madhuri Datta1,2,#, Adrita Banerjee1,2, Aindrila Chattopadhyay2
    BIOCELL, DOI:10.32604/biocell.2026.075963
    (This article belongs to the Special Issue: Melatonin and Mitochondria: Exploring New Frontiers)
    Abstract Non-steroidal anti-inflammatory drugs (NSAIDs) are widely prescribed, but their long-term use frequently results in gastric mucosal injury. Emerging evidence indicates that, beyond cyclooxygenase inhibition, mitochondrial dysfunction represents a central mechanism driving NSAID-induced gastric epithelial damage. This review aims to critically synthesize current evidence on mitochondria-centered pathways involved in NSAID-induced gastric ulceration and to evaluate the therapeutic relevance of melatonin in this context. We highlight how NSAIDs impair mitochondrial bioenergetics, promote excessive reactive oxygen species generation, disrupt membrane potential, and activate apoptotic signaling, thereby compromising mucosal integrity. Importantly, melatonin exerts multifaceted gastroprotective actions by preserving mitochondrial More >

  • Open Access

    REVIEW

    Emerging Role of ACOD1/Itaconate in Cancer: Bridging Metabolic Reprogramming and Signaling in the Tumor Microenvironment

    Xing-Guo Li1,2,3,#, Lu-Kai Wang4,#, Fu-Ming Tsai5, Hsueh-Chun Wang1,*
    BIOCELL, DOI:10.32604/biocell.2026.075492
    (This article belongs to the Special Issue: Natural and Synthetic Small Molecules in the Regulation of Immune Cell Functions)
    Abstract Itaconate, produced by aconitate decarboxylase 1 (ACOD1, also known as IRG1), acts as a key immunometabolite that inhibits succinate dehydrogenase (SDH) and can engage reduction-oxidation (redox)-sensitive signaling programs. This review summarizes the emerging, context-dependent roles of the ACOD1-itaconate axis in cancer, while critically distinguishing between the effects of endogenous itaconate and its cell-permeable derivatives. In tumor cells, endogenous ACOD1 expression or uptake via solute carrier family 13 member 3 (SLC13A3) alters oxidative phosphorylation and glycolysis. In the tumor microenvironment, myeloid-derived itaconate contributes to immune tolerance by reducing dendritic-cell cross-priming and limiting CD8+ T-cell metabolic activity. Moreover, More >

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