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  • 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 >

  • Open Access

    ARTICLE

    Dexmedetomidine Protects Intestinal Mucosal Barrier via Activating the α7-nAChR-GDNF in Enteric Glial Cells

    Yuanhong Mao#, Yunlan Yang#, Kun Yang§, Yongqiang Sun, Kun Yang*

    BIOCELL, Vol.50, No.3, 2026, DOI:10.32604/biocell.2026.075138 - 23 March 2026

    Abstract Objective: Intestinal barrier disruption is a critical event in sepsis and ischemia–reperfusion (I/R) injury. Enteric glial cells (EGCs) maintain barrier integrity by secreting glial cell line–derived neurotrophic factor (GDNF). This study aimed to determine whether Dexmedetomidine (Dex) protects the intestinal barrier via α7-nicotinic acetylcholine receptor (α7-nAChR) signaling in EGCs. Methods: An in vitro EGC-intestinal epithelial cell (IEC) co-culture system and a murine intestinal I/R model were established. EGCs were selectively ablated in vivo using benzalkonium chloride (BAC). Barrier integrity was evaluated by transmembrane electrical resistance (TEER) and plasma FITC-dextran permeability. Enzyme-Linked Immunosorbent Assay (ELISA) and Western blotting… More >

  • Open Access

    ARTICLE

    BORIS/CTCFL Reprograms Glioblastoma Transcriptional Networks through the Regulation of Tumor-Associated Genes such as CD36 and FBN2

    Gerardo Ramírez-Mejía1,#, Sofía Plata-Burgos1,#, Raquel Cuevas-Díaz Duran2, Adrian Ledesma-Beiza1, Cynthia Sámano1, Thalía Estefanía Sánchez-Correa3, Ernesto Soto-Reyes1,*

    BIOCELL, Vol.50, No.3, 2026, DOI:10.32604/biocell.2026.075061 - 23 March 2026

    Abstract Objectives: Glioblastoma multiforme (GBM) is a highly aggressive brain tumor characterized by extensive transcriptional and epigenetic dysregulation. Brother of the Regulator of Imprinted Sites (BORIS/CTCFL) has been implicated in oncogenic transcriptional programs in several cancers, but its role in GBM remains poorly defined. This study aimed to characterize BORIS-associated transcriptional programs in GBM and to assess their functional relevance using integrative computational and experimental approaches. Methods: Transcriptomic data from The Cancer Genome Atlas (TCGA)-GBM and Genotype-Tissue Expression (GTex) brain cortex were analyzed following batch correction, differential expression analysis, and gene ontology enrichment. TCGA-GBM samples were… More >

  • Open Access

    ARTICLE

    Melatonin Ameliorates Hippocampal Excitotoxicity and Neuroinflammation in Permanent MCAO by Targeting NMDA/AMPA Receptors and the NLRP3 Inflammasome via Nrf2/PPARγ/JNK/NF-κB Crosstalk

    Abdullah Alattar1, Reem Alshaman1, Fawaz E. Alanazi1, Yusuf S. Althobaiti2, Ghareb M. Soliman3, Waleed Salman Khubrni1, Howaida S. Ali4, Fawad Ali Shah5,6,*

    BIOCELL, Vol.50, No.3, 2026, DOI:10.32604/biocell.2026.074865 - 23 March 2026

    Abstract Objectives: Permanent middle cerebral artery occlusion (pMCAO) can lead to hippocampal damage through multiple linked pathways such as reactive oxidative stress (ROS), neuroinflammation mediated by NOD-, LRR- and pyrin domain-containing protein 3 (NLRP3), tumour necrosis factor-alpha (TNF-α), and nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB), and glutamate excitotoxicity involving N-methyl-D-aspartate receptor subunits 2a and 2b (NR2a/NR2b) and α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptor (AMPAR/GluR1). The hippocampus, which is essential for memory and cognition, is at a substantial risk of ischemic degeneration. The aim of this study was to investigate the neuroprotective potential of melatonin in regulating these… More > Graphic Abstract

    Melatonin Ameliorates Hippocampal Excitotoxicity and Neuroinflammation in Permanent MCAO by Targeting NMDA/AMPA Receptors and the NLRP3 Inflammasome via Nrf2/PPAR<b>γ</b>/JNK/NF-<b>κ</b>B Crosstalk

  • Open Access

    ARTICLE

    ERK- and p53-Mediated ATF3 Expression Contributes to Cisplatin-Induced DNA Damage in Renal Epithelial Cells

    Semin Lee1,2,#, Minjun Kim3,4,#, Seungmin Lee2,5, Jiyun Yoo1,5, Soo Seok Hwang6,7, Seongchan Kim8, Seung Pil Yun9,10, Dong Kyu Choi11,12,*, Sangdun Choi13,14,*, Hyuk-Kwon Kwon1,2,5,*

    BIOCELL, Vol.50, No.3, 2026, DOI:10.32604/biocell.2026.074555 - 23 March 2026

    Abstract Objective: Cisplatin is a widely used chemotherapeutic agent due to its ability to damage DNA in the treatment of cancer. However, its clinical application is often limited by adverse effects on normal tissues, especially the kidneys. Understanding the molecular mechanisms of cisplatin-induced nephrotoxicity is crucial for developing strategies to mitigate its side effects. In this study, we aimed to elucidate the molecular mechanisms underlying cisplatin-induced DNA damage and apoptosis in human renal epithelial cells, with a focus on key signaling pathways and mediators that drive nephrotoxicity. Methods: To explore these mechanisms, human proximal tubule epithelial… More >

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