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  • Open Access

    ARTICLE

    ETS1 Regulates Endothelial AQP1 Expression via Interaction with MEF2C in Endothelial Cells

    Yong Jiang*, Rui Ma, Yu-Ge Wu, Yi-Ming Huo, Han-Zhu Zhou, Jun-Xuan Zhang

    BIOCELL, Vol.50, No.4, 2026, DOI:10.32604/biocell.2026.075982 - 21 April 2026

    Abstract Background: Aquaporin 1 (AQP1) plays a key role in myocardial ischemia-reperfusion (I/R) injury. This study aimed to elucidate the mechanisms by which erythroblast transformation-specific 1 (ETS1) and myocyte enhancer factor 2C (MEF2C) regulated AQP1 transcription. Methods: Human umbilical vein endothelial cells (HUVECs) and rats with coronary heart disease were employed for in vitro and in vivo experiments, respectively. Expressions of ETS1, MEF2C, and AQP1 were analyzed by western blotting and quantitative reverse transcription polymerase chain reaction (qRT-PCR). Chromatin immunoprecipitation (ChIP) and co-immunoprecipitation (Co-IP) assays were performed to confirm the interactions between ETS1 and MEF2C. Scratch wound healing and… More > Graphic Abstract

    ETS1 Regulates Endothelial AQP1 Expression via Interaction with MEF2C in Endothelial Cells

  • Open Access

    ARTICLE

    Research on the Mechanism of Gallic Acid Inhibiting Ferroptosis and Delaying IgA Nephropathy by Regulating the MAPK Signaling Pathway through DUSP1

    Qiguo Wang1, Qin Wang2, Wen Ye3, Qin Feng3, Ting Wang3,*

    BIOCELL, Vol.50, No.4, 2026, DOI:10.32604/biocell.2026.075633 - 21 April 2026

    Abstract Objectives: IgA nephropathy (IgAN) is a common primary glomerulonephritis with limited treatment options. Gallic acid (GA) has demonstrated renal protective effects, but its precise mechanisms against IgAN remain incompletely elucidated. This study aims to reveal the molecular mechanism by which GA exerts a renal protective effect on IgAN. Methods: Transcriptomics and network pharmacology were combined in an integrative manner. The GSE175759 dataset’s differentially expressed genes (DEGs) were filtered out. SwissTargetPrediction and Traditional Chinese Medicine Systems Pharmacology Database and Analysis Platform (TCMSP) were used to forecast GA’s goals. Core targets and pathways were obtained by functional… More >

  • Open Access

    REVIEW

    Research Advances and Therapeutic Potential of Gut Microbiota in Metabolic Diseases

    Shuyu Yuan1,#, Guoxiao Han1,#, Huimin Qiu1, Henan Zheng2, Rongzhi Fang1, Wangmiao Xie1, Wangui Yu1,*, Xiaochun Peng1,*

    BIOCELL, Vol.50, No.4, 2026, DOI:10.32604/biocell.2026.075338 - 21 April 2026

    Abstract The gut microbiota plays a pivotal role in maintaining host metabolic homeostasis. Accumulating evidence has demonstrated that dysbiosis of the gut microbiota is closely associated with metabolic disorders, including obesity, type 2 diabetes mellitus (T2DM), and non-alcoholic fatty liver disease (NAFLD). These alterations affect energy harvest, bile acid and short-chain fatty acid metabolism, intestinal barrier integrity, and low-grade inflammation, thereby contributing to insulin resistance and ectopic fat accumulation. In this narrative review, we summarize current knowledge on microbiome-host interactions in metabolic diseases, with a focus on energy metabolism, immune regulation, and inflammatory pathways. We further More > Graphic Abstract

    Research Advances and Therapeutic Potential of Gut Microbiota in Metabolic Diseases

  • Open Access

    ARTICLE

    SOX11 Alleviates Osteoarthritis through Reducing Mitochondrial Dysfunction and Ferroptosis via Binding to the Promoter of NOX4

    Xingchang Fu, Gang Yang*

    BIOCELL, Vol.50, No.4, 2026, DOI:10.32604/biocell.2026.074951 - 21 April 2026

    Abstract Objectives: Mitochondrial dysfunction and ferroptosis play crucial roles in osteoarthritis (OA), but the mechanisms remain unclear. This study aims to investigate the mechanism of sex-determining region Y-box transcription factor (SOX) 11/nicotinamide adenine dinucleotide phosphate (NADPH) oxidase 4 (NOX4) axis-mediated mitochondrial dysfunction and ferroptosis in OA. Methods: Destabilization of the medial meniscus (DMM) induced knee OA in mice. Chondrocytes were stimulated with IL-1β. Ferroptosis and mitochondrial function-related indicators were detected by immunofluorescence, 5,5,6,6-Tetrachloro-1,1,3,3-tetraethyl-imidacarbocyanine iodide (JC-1) staining, flow cytometry, quantitative real-time polymerase chain reaction (qRT-PCR), and Western blot. Results: OA mice had 4.4 and 1.1-fold increase in SOX11… More > Graphic Abstract

    SOX11 Alleviates Osteoarthritis through Reducing Mitochondrial Dysfunction and Ferroptosis via Binding to the Promoter of NOX4

  • Open Access

    REVIEW

    Molecular Mechanisms and Signaling Pathways of Myocardial Ischemia: A Multidimensional Analysis from Energy Metabolism to Cell Death

    Yiwei Hao1,#, Yaodong Ping2,#, Yan Yang3, Cheng Qu3, Yuan Chen1, Xueyan Jiang1, Rong Fu1, Hailong Zhao4,*, Lei Yu4,*

    BIOCELL, Vol.50, No.4, 2026, DOI:10.32604/biocell.2025.074863 - 21 April 2026

    Abstract Myocardial ischemia, a core pathological process underlying diverse cardiovascular diseases such as coronary artery disease, poses a severe threat to global human health by frequently leading to acute myocardial infarction, heart failure, and even sudden cardiac death. A comprehensive understanding of its intricate underlying pathogenic mechanisms is not only crucial for developing effective therapeutic strategies but also essential for accelerating the translation of basic research findings into clinical practice. However, the complex regulatory networks that drive myocardial ischemia remain to be systematically clarified. These networks encompass the intricate interactions among multiple pathological processes, including energy… More >

  • Open Access

    PROTOCOL

    Flow Cytometry Study of Immune Cell Subpopulations from the Mouse Vertebral Bone Marrow and Intervertebral Disc Following Endplate Microfracture

    Dalin Wang1, Mingcai Zhang1, Richard Hastings2, Patrick George1, Ryan Ranzau1, Jinxi Wang1,3,*

    BIOCELL, Vol.50, No.4, 2026, DOI:10.32604/biocell.2026.074572 - 21 April 2026

    Abstract Objective: Although endplate (EP) injury may cause intervertebral disc (IVD) degeneration and Modic changes (MCs) in the vertebral bone marrow (VBM), EP injury-induced synchronous cellular reactions and their crosstalk in the IVD and VBM remain unclear. This protocol-based study aimed to streamline and optimize the methods of tissue harvest and cell preparation for flow cytometry (FCM) analysis of T-cell and macrophage subpopulations in both VBM and IVD adjacent to the surgically induced EP microfracture in mice. Methods: EP injury or sham procedure was performed at the spinal levels L4-5 and L5-6 in male mice. Step-by-step… More >

  • Open Access

    ARTICLE

    KDM6B Regulates the Tumor Microenvironment and Promotes EMT via the PI3K/AKT/mTOR Signaling in Differentiated Thyroid Cancer

    Jiangtao Yu*, Qingfeng Huo, Xinxin Duan

    BIOCELL, Vol.50, No.4, 2026, DOI:10.32604/biocell.2026.073331 - 21 April 2026

    Abstract Objectives: The tumor microenvironment and epithelial-mesenchymal transition (EMT) are closely linked to the progression of differentiated thyroid cancer (DTC). However, the functional mechanisms of lysine-specific demethylase 6B (KDM6B) in carcinogenesis remain incompletely understood. This study aims to clarify whether KDM6B affects DTC progression and EMT through the phosphatidylinositol 3-kinase/protein kinase B/mammalian target of the rapamycin (PI3K/AKT/mTOR) pathway, providing a potential target for clinical treatment of DTC. Methods: Tissue samples from DTC patients (n = 39) were collected, and KDM6B expression was determined through Reverse Transcription-Polymerase Chain Reaction (RT-PCR) and Western blot. Cell counting kit-8 assay, 5-Ethynyl-2-deoxyuridine… More > Graphic Abstract

    KDM6B Regulates the Tumor Microenvironment and Promotes EMT via the PI3K/AKT/mTOR Signaling in Differentiated Thyroid Cancer

  • Open Access

    REVIEW

    Targeting Inflammation in Coronary Artery

    Michael I. Bukrinsky1, Alessio L. Ravani2, Anastasia V. Poznyak3,*

    BIOCELL, Vol.50, No.4, 2026, DOI:10.32604/biocell.2026.072752 - 21 April 2026

    Abstract Atherosclerosis (AS) is a key contributor to ischemic heart disease, resulting in significant cardiovascular (CV) morbidity and mortality worldwide. Despite advancements in managing conventional risk factors, including the utilization of statins, recurrent adverse cardiovascular events remain prevalent, emphasizing the need for novel therapeutic strategies. This review explores the critical role of inflammation in the pathogenesis of coronary artery disease (CAD) and highlights potential atheroprotective approaches targeting inflammatory pathways. We discuss the multifaceted interplay between immune responses and AS, detailing the contributions of myeloid cells, T lymphocytes, and various cytokines in plaque formation and instability. Recent More >

  • Open Access

    REVIEW

    Targeting Protein Arginine Deiminases in Rheumatoid Arthritis: Pathophysiology and Therapeutic Progress

    Yung-Chieh Huang1,2,3, Wen-Chien Cheng4,5, Ya-Hsuan Chao6, Tzu-Ting Chen7,*, Chi-Chen Lin8,9,10,11,*

    BIOCELL, Vol.50, No.4, 2026, DOI:10.32604/biocell.2025.072732 - 21 April 2026

    Abstract Protein arginine deiminases (PADs) are key enzymes in the development of rheumatoid arthritis (RA), catalyzing the conversion of arginine to citrulline in a process called citrullination. This post-translational modification is crucial to RA pathogenesis as it creates neo-antigens that trigger the production of anti-citrullinated protein antibodies (ACPAs). These ACPAs are highly specific to RA and often appear before clinical symptoms, making them valuable biomarkers for diagnosis and prognosis. Beyond ACPA production, PADs, particularly PAD4, play a vital role in forming neutrophil extracellular traps (NETs). NETs contribute to inflammation and joint damage, further highlighting the importance… More > Graphic Abstract

    Targeting Protein Arginine Deiminases in Rheumatoid Arthritis: Pathophysiology and Therapeutic Progress

  • Open Access

    REVIEW

    The Therapeutic Potential of iNKT Cells in the Treatment of Ovarian Cancer

    Anna PawłOwska-ŁAchut*, Dorota Suszczyk, Iwona Wertel

    BIOCELL, Vol.50, No.4, 2026, DOI:10.32604/biocell.2025.072104 - 21 April 2026

    Abstract Ovarian cancer (OC) remains the most lethal gynecological malignancy, and it is characterized by high heterogeneity, early metastatic dissemination, and frequent recurrence within 12–18 months after primary therapy. Despite progress in clinical management and drug development, the mortality rate remains high, and the biological drivers of OC aggressiveness are not fully understood. A major contributor to therapeutic resistance and disease progression is the ovarian tumor microenvironment (TME), which supports tumor growth and immune evasion. Its complexity poses significant challenges to the development of effective therapies. Current treatments, especially in advanced or recurrent stages, have limited… More >

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