Open Access
ISSN:0327-9545 (print)
ISSN:1667-5746 (online)
Publication Frequency:Monthly
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.
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
COMMENTARY
BIOCELL, Vol.50, No.10, 2026, DOI:10.32604/biocell.2026.080846 - 22 September 2026
（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
BIOCELL, Vol.50, No.10, 2026, DOI:10.32604/biocell.2026.082812 - 22 September 2026
（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
BIOCELL, Vol.50, No.10, 2026, DOI:10.32604/biocell.2026.081123 - 22 September 2026
（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
BIOCELL, Vol.50, No.10, 2026, DOI:10.32604/biocell.2026.083756 - 22 September 2026
（This article belongs to the Special Issue: Modulation of Inflammation, Oxidative Stress, and Mitochondrial Function: Therapeutic Perspectives Across Diseases)
Abstract Oxidative stress results from an imbalance between reactive oxygen species (ROS) production and antioxidant defense mechanisms and contributes to cellular damage and the pathogenesis of various diseases. This review summarizes recent advances in the molecular and biochemical mechanisms associated with oxidative stress in ocular diseases, including dry eye disease, diabetic retinopathy, age-related macular degeneration (AMD), glaucoma, and cataract. A literature search was conducted using PubMed and Google Scholar databases to identify relevant studies published up to 31 December 2025. Current evidence suggests that oxidative stress plays an important role in inflammation, mitochondrial dysfunction, and cellular More >
Open Access
REVIEW
BIOCELL, Vol.50, No.10, 2026, DOI:10.32604/biocell.2026.081268 - 22 September 2026
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
REVIEW
BIOCELL, Vol.50, No.10, 2026, DOI:10.32604/biocell.2026.081112 - 22 September 2026
（This article belongs to the Special Issue: Cellular and Molecular Mechanisms of Gut Microbiota, Oxidative Stress, and Inflammation in Health and Disease)
Abstract Type 1 diabetes (T1D) is traditionally described as a T cell–mediated autoimmune disease, yet accumulating longitudinal evidence indicates that metabolic and environmental perturbations—including depletion of short-chain fatty acid (SCFA)–producing gut microbiota—precede seroconversion and overt autoimmunity. We propose that SCFA loss represents an upstream trigger of endocannabinoid system (ECS) imbalance in T1D. Integrating evidence from microbiome, lipid signaling, mitochondrial biology, and immunometabolic research, we construct a mechanistic model in which reduced SCFA availability impairs lipid homeostasis and promotes overproduction of 2-arachidonoylglycerol (2-AG), potentially driving cannabinoid receptor 1 (CB1) dominance and receptor asymmetry. The resulting arachidonic acid More >
Open Access
REVIEW
BIOCELL, Vol.50, No.10, 2026, DOI:10.32604/biocell.2026.081324 - 22 September 2026
（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
BIOCELL, Vol.50, No.10, 2026, DOI:10.32604/biocell.2026.082448 - 22 September 2026
（This article belongs to the Special Issue: Autophagy and Oxidative Stress in Cancer: Molecular Crossroads and Cell Fate Decisions)
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
BIOCELL, Vol.50, No.10, 2026, DOI:10.32604/biocell.2026.081318 - 22 September 2026
（This article belongs to the Special Issue: Advanced Cell Signaling Pathways in Health and Disease)
Abstract Objectives: Tumor-associated macrophages (TAMs) within the hypoxic tumor microenvironment critically drive colorectal cancer (CRC) progression, yet their specific regulatory mechanisms on endoplasmic reticulum (ER) homeostasis via microRNAs remain understood. This study aims to assess the impact of hypoxia-induced TAMs on CRC cells through the microRNA-320 (miR-320)/SRY-box transcription factor 4 (SOX4) axis, focusing on ER homeostasis and malignant behaviors. Methods: Human CRC cell lines HCT116 and SW480 were co-cultured with hypoxia-induced macrophages. Cells were treated with miR-320 mimics and inhibitors to evaluate proliferation and apoptosis using Cell-counting kit-8 (CCK8) assays and flow cytometry. Western blotting was performed… More >
Open Access
ARTICLE
BIOCELL, Vol.50, No.10, 2026, DOI:10.32604/biocell.2026.081934 - 22 September 2026
Abstract Objective: Periodontal diseases can cause pro-inflammatory cytokine overproduction, particularly tumor necrosis factor-alpha (TNF-α), and this inflammatory microenvironment is a critical driver of oral cancer progression. MicroRNA-146a-5p is a key regulator of inflammation, linked to both periodontal disease and carcinogenesis. The objective of this study was to illustrate the regulatory function of miR-146a-5p in gingival squamous cell carcinoma OECM-1 cells under conditions that mimic those of periodontal disease. Methods: OECM-1 cells were stimulated with 25 ng/mL TNF-α for 48 h, and subsequently transfected with 50 nM miR-146a-5p mimic or inhibitor for an additional 48 h. The inflammatory… More >
Open Access
ARTICLE
BIOCELL, Vol.50, No.10, 2026, DOI:10.32604/biocell.2026.082951 - 22 September 2026
Abstract Background: Macrophage-derived eicosanoids are involved in airway inflammation associated with asthma, but the mechanisms regulating their production remain incompletely understood. The study aimed to evaluate the effects of isorhynchophylline (IRN) on eicosanoid production and inflammatory activation in LPS/IFN-γ-stimulated THP-1-derived macrophages and to further investigate whether these effects are mediated through the miR-200a/FOXC1/NF-κB axis. Methods: THP-1 cells were differentiated into M0 (PMA) and polarized into M1 (LPS+IFN-γ) phenotypes. IRN (5–20 μM) was applied. Eicosanoids (PGE2, LTB4) were measured via ELISA; COX-2, 5-LOX, mPGES-1, FOXC1, p-IκBα/IκBα, and p-p65/p65 were measured via Western blotting; and miR-200a and target genes were… More >
Open Access
ARTICLE
BIOCELL, Vol.50, No.10, 2026, DOI:10.32604/biocell.2026.085300 - 22 September 2026
Abstract Background: Volatile anesthetics such as sevoflurane are ubiquitous in perioperative care, yet their unintended consequences on pulmonary microvascular integrity and the upstream intracellular signaling pathways remain incompletely defined. This study elucidates the precise transcriptional mechanisms linking sevoflurane exposure to pulmonary endothelial hyperpermeability. Methods: Transendothelial electrical resistance (TEER) and macromolecular permeability were dynamically quantified in human pulmonary microvascular endothelial cell (HPMEC) monolayers following sevoflurane exposure. Global transcriptomic profiling (RNA-seq) was employed to identify core regulatory nodes, which were functionally validated via targeted siRNA silencing in vitro and subsequently corroborated in a murine model of clinical sevoflurane inhalation. Results: Sevoflurane… More >
Open Access
ARTICLE
BIOCELL, Vol.50, No.10, 2026, DOI:10.32604/biocell.2026.081668 - 22 September 2026
Abstract Objectives: Middle ear cholesteatoma (MEC) is a destructive and locally invasive disease that leads to erosion of bone structure and serious complications. This study aimed to investigate the role of GDF11 in promoting the differentiation of macrophages into osteoclasts in vitro and elucidate the bone erosion mechanism in MEC. Methods: The MEC dataset GSE116142 was subjected to bioinformatics analysis. The Growth Differentiation Factor 11 (GDF11) and Transforming Growth Factor Beta Receptor 1 (TGFBR1) expression levels in MEC were evaluated using immunohistochemical analysis. RAW264.7 cells were induced with different concentrations of recombinant GDF11 (rGDF11) with or without the… More >
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