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BIOCELL | An Open Access Journal from Tech Science Press

BIOCELL Open Access

BIOCELL

ISSN:0327-9545 (print)
ISSN:1667-5746 (online)
Publication Frequency:Monthly

  • Online
    Articles

    2361

  • on board
    editors

    64

Special Issues
Table of Content


About the Journal

BIOCELL is an international, peer-reviewed, open access journal on molecular and cellular biosciences. The journal welcomes high quality original research articles, review papers, communications, perspectives, commentaries, etc. Topics of interest include but are not limited to: Cellular Biochemistry, Structural & Molecular Biology, Cellular/Molecular Biology, Immunology, Pathology & Neurobiology, Cell Signaling, Regenerative Biology & Stem Cells, Cancer Biology, RNA Biology, Genomics, Transcriptomics, Proteomics & Metabolomics, Plant Molecular & Cellular Biology.

Indexing and Abstracting

Science Citation Index Expanded (SCIE): 2025 Impact Factor 1.8; Journal Citation Report/Science Edition (JCR); Scopus; Scopus Citescore (Impact per Publication 2025): 2.7; SNIP (Source Normalized Impact per Paper 2025): 0.298; Sociedad Argentina de Investigaciones en Bioquímica y Biología Molecular (SAIB); Portico, etc.

  • Open Access

    REVIEW

    Short-Chain Fatty Acids and Related Postbiotic Mediators in Neurodegenerative Diseases

    Shazia Ansari1, Gursimran Singh1, Jemimol Solomon1, Simranpreet Kaur1, Khadga Raj Aran1,2,*

    BIOCELL, Vol.50, No.11, 2026, DOI:10.32604/biocell.2026.082358 - 19 October 2026
    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

    REVIEW

    Astrocyte- and Microglia-Derived Factors in Neuroinflammation: Impact on Neuronal and Synaptic Structure and Function

    Giuliana Colonna Soldavini1,2,#, María Belén Gomez1,#, Jeremias Martin Cuello1,2, Martín Gabriel Codagnone1,2, Analía Gabriela Reinés1,2,*

    BIOCELL, Vol.50, No.11, 2026, DOI:10.32604/biocell.2026.082340 - 19 October 2026
    (This article belongs to the Special Issue: Advanced Cell Signaling Pathways in Health and Disease)
    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

    The Intersection of Impaired Ion Channels and Depleted Mitochondria in Epileptic Seizures: A Narrative 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, Vol.50, No.11, 2026, DOI:10.32604/biocell.2026.081478 - 19 October 2026
    (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

    Gut Microbiota, Oxidative Stress, and Extracellular Vesicles: Molecular Crosstalk in Inflammation and Disease and Therapeutic Interventions

    Hassan Ali1,2,3, Tsvetelina Velikova3,*, Petya Marinova3

    BIOCELL, Vol.50, No.11, 2026, DOI:10.32604/biocell.2026.081372 - 19 October 2026
    (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

    NRF2 Insufficiency in Chronic Disease

    José Manuel Pérez de la Lastra1,*, Celia María Curieses Andrés2, Elena Bustamante Munguira2, Celia Andrés Juan3, Eduardo Pérez Lebeña4

    BIOCELL, Vol.50, No.11, 2026, DOI:10.32604/biocell.2026.080868 - 19 October 2026
    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

    The Autophagy-Oxidative Stress Circuit: A Conductor of Cell Fate

    Yi Lu1,#, Lixiang Wang1,#, Jiaheng Xu1,#, Heru Wang1, Jiayu Li1, Wanshun Li1, Xinyi Su1, Hongyu Li2, Deyu Zhang1,*, Zhendong Jin1,*, Haojie Huang1,*

    BIOCELL, Vol.50, No.11, 2026, DOI:10.32604/biocell.2026.082978 - 19 October 2026
    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

    Metformin as a Geroprotective Agent: Multifaceted Mechanisms Targeting Cellular Senescence and Aging Hallmarks

    Yiting Zhao, Lei Gao*

    BIOCELL, Vol.50, No.11, 2026, DOI:10.32604/biocell.2026.083060 - 19 October 2026
    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

    GNA13 Regulates the β-Catenin Pathway to Promote Esophageal Cancer Cell Invasion while Inhibiting Apoptosis

    Xu Chen*, Zhen Wang, Qing Hu

    BIOCELL, Vol.50, No.11, 2026, DOI:10.32604/biocell.2026.084368 - 19 October 2026
    Abstract Background: G protein subunit alpha 13 (GNA13) plays a role in the progression of many malignant tumors, but its expression in esophageal carcinoma (ESCA) cells and impact on their biological behavior are unknown. This research aims to clarify the functions and mechanisms of GNA13 on the malignant phenotype of ESCA cells. Methods: GNA13 expression in ESCA tissues and cells was assessed using reverse transcription quantitative polymerase chain reaction (RT-qPCR) and Western blot. Sh-GNA13 was transfected into ESCA cells (TE-1 and KYSE-150) to assess the efficiency of GNA13 silencing. The effects of GNA13 silencing on cell viability,… More >

  • Open Access

    ARTICLE

    CircATRNL1 Facilitates Malignant Progression of Non–Small Cell Lung Cancer via the miR-103a-3p/IGFBP3/PI3K-AKT Axis

    Jiawei Liu1,2,3,#, Tao Huang2,3,#, Qi You2, Yuxiang Cao4, Shaojin Zhu2,3,*, Feng Liu1,5,*

    BIOCELL, Vol.50, No.11, 2026, DOI:10.32604/biocell.2026.085464 - 19 October 2026
    Abstract Background: Circular RNAs have emerged as important regulators of non-small cell lung cancer progression through competing endogenous RNA networks, but the specific role and mechanism of CircATRNL1 in NSCLC remain unclear. This study investigates the mechanistic role of CircATRNL1 in the malignant progression of non-small cell lung cancer (NSCLC). Methods: Gene expression levels in NSCLC cell lines were quantified using reverse transcription quantitative PCR (RT-qPCR). Functional assays, including Western blot analysis of epithelial–mesenchymal transition (EMT)-related proteins, wound-healing assays, and Transwell migration and invasion assays, were performed to assess the effects of CircATRNL1 on cellular motility and… More >

  • Open Access

    ARTICLE

    Effect of LncRNA UFC1 Downregulation on Alleviating Glucocorticoid Resistance in Chronic Obstructive Pulmonary Disease via the PI3K/AKT Pathway

    Jingjing Wu, Jing Wang, Yufeng Wan*, Yue Li*

    BIOCELL, Vol.50, No.11, 2026, DOI:10.32604/biocell.2026.086220 - 19 October 2026
    Abstract Background: Chronic obstructive pulmonary disease (COPD) is a chronic inflammatory airway disease frequently complicated by glucocorticoid (GC) resistance. This study investigated whether lncRNA UFC1 regulates cigarette smoke extract (CSE)-induced inflammation, apoptosis, and GC resistance through phosphatidylinositol 3-kinase/protein kinase B (PI3K/AKT) signaling. Methods: To simulate cellular damage and GC insensitivity in vitro, U937 cells were subjected to CSE stimulation. The influence of lncRNA UFC1 silencing on cell survival, inflammatory responses, apoptosis, and GC responsiveness was evaluated through a combination of Cell Counting Kit-8 (CCK-8), reverse transcription quantitative polymerase chain reaction (RT-qPCR), enzyme-linked immunosorbent assay (ELISA), Western blot, flow… More >

    Graphic Abstract

    Effect of LncRNA UFC1 Downregulation on Alleviating Glucocorticoid Resistance in Chronic Obstructive Pulmonary Disease via the PI3K/AKT Pathway

  • Open Access

    ARTICLE

    Luteolin Reverses Methotrexate Resistance in Rheumatoid Arthritis via Targeting Sp1-DHFR Axis and p38 MAPK/STAT3 Signaling

    Zheng Zhang1,2, Qingchun Huang1,*

    BIOCELL, Vol.50, No.11, 2026, DOI:10.32604/biocell.2026.083358 - 19 October 2026
    Abstract Background: Rheumatoid arthritis (RA) is a disabling autoimmune disease where methotrexate resistance, driven by Specificity protein 1 (Sp1)-mediated upregulation of dihydrofolate reductase, poses a key clinical challenge. Preliminary network pharmacology analysis identified Dihydrofolate reductase (DHFR) as a high-confidence target of luteolin in RA. Given that Sp1 is a known transcriptional activator of DHFR, we further investigated whether luteolin modulates the DHFR-Sp1 axis, thereby prompting this study to explore its potential in overcoming Methotrexate (MTX) resistance. Methods: An MTX-resistant human fibroblast-like synoviocyte (FLS) model was established in vitro to investigate whether luteolin can reverse MTX resistance and elucidate… More >

  • Open Access

    ARTICLE

    Mdfi Regulates Myoblast Proliferation and Cell Cycle Progression through Cyclins

    Yiren Jiao1,*, Lingbo Cao2, Jing Xu1, Hongkai Sun1, Jia Shi3, Xiaoli Ma1, Zehao Wang1,*, Baozhen Zhou1,*

    BIOCELL, Vol.50, No.11, 2026, DOI:10.32604/biocell.2026.083738 - 19 October 2026
    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 >

Copyright © 2026 The Author(s). Published by Tech Science Press.

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