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  • Open Access

    ARTICLE

    CNPY2 Regulates Macrophage Polarization and Inflammatory Immune Responses via the TLR4/NF-κB Signaling Pathway to Alleviate Osteomyelitis of the Jaw

    Rihui Wang1,2,#, Wanlu Li3,#, Canyang Jiang1,2, Jianping Huang1,2, Kangwei Zhou1,2, Yan Jiang4,5, Junyang Zhang1,2, Li Huang1,2,*

    BIOCELL, Vol.50, No.5, 2026, DOI:10.32604/biocell.2026.075875 - 13 May 2026

    Abstract Background: Osteomyelitis of the jaw (OMJ) is a severe infectious bone disease. While Canopy FGF signaling regulator 2 (CNPY2) is known to regulate inflammatory diseases, its role in OMJ remains unclear. The study aimed to investigate the role of CNPY2 in the mandibular joint and its molecular mechanisms. Methods: An in vitro OMJ model was generated by stimulating RAW264.7 macrophages with S. aureus. CNPY2 knockdown and overexpression models were established using siRNA and plasmids. Functional assays assessed cell proliferation, migration, and invasion. Macrophage polarization, cytokine secretion, and osteoclast differentiation were analyzed. The CNPY2-Toll-Like Receptor 4 (TLR4)/Nuclear factor-kappa B… More > Graphic Abstract

    CNPY2 Regulates Macrophage Polarization and Inflammatory Immune Responses via the TLR4/NF-κB Signaling Pathway to Alleviate Osteomyelitis of the Jaw

  • Open Access

    ARTICLE

    Synergistic Cell Death: Cisplatin Inflames Tumors by Coordinating Multiple Death Programs

    Ju Li1, Pengcheng Rao1, Dan Yang1, Tong Zhou1, Jianguo Gan1, Die Lv1, Shuting Zhou1, Yang Peng1, Xiaoqiang Xia1, Qianming Chen1, Yuchen Jiang1, Jian Jiang2, Xiaoping Xu1,*, Xiaodong Feng1,*

    BIOCELL, Vol.50, No.5, 2026, DOI:10.32604/biocell.2026.075437 - 13 May 2026

    Abstract Objective: Multiple programmed cell death (PCD) pathways have been individually reported to be triggered by cisplatin, but whether and how they are co-regulated remains unclear. In this study, we comprehensively investigate the spectrum of cisplatin-induced PCD. Methods: We employed integrated in vitro and in vivo models, including human cancer cell lines, a Cal27 xenograft mouse model, and paired clinical specimens from an oral squamous cell carcinoma patient receiving neoadjuvant cisplatin-based chemotherapy. A comprehensive methodological suite-encompassing cell death assays, Western blotting, Hematoxylin and eosin staining, immunofluorescence, Cyclic multiplexed tissue staining, and pathway-specific pharmacological inhibitors was utilized to dissect the… More >

  • Open Access

    REVIEW

    Receptor Reexpression after Hypermethylation: Novel Targets for Inhibitors and Antibody-Drug Conjugates in ALL

    Christoph Rehbach1, Patrick A. H. Ehm2,*

    BIOCELL, Vol.50, No.5, 2026, DOI:10.32604/biocell.2026.075170 - 13 May 2026

    Abstract Despite improved overall prognosis, the treatment of high-risk acute lymphoblastic leukemia (ALL) remains challenging due to the toxicity of intensive polychemotherapy and the limited efficacy of antibody-targeted therapies beyond cluster of differentiation 20 and 22 (CD20 and CD22). ALL is driven not only by genetic alterations but also by profound epigenetic dysregulation, including promoter hypermethylation that also silences surface receptor genes. This epigenetic repression can reduce the efficacy of targeted immunotherapies and contribute to relapse. Epigenetic reprogramming with DNA demethylating agents (e.g., decitabine) has the potential to restore the expression of key B cell receptors… More >

  • Open Access

    ARTICLE

    Anti-Inflammatory Effects of Veratramine against Lipopolysaccharide-Induced Inflammation

    Gyuri Han#, Yun Hee Jeong#, Ga Eun Kim, Jong-Sup Bae*

    BIOCELL, Vol.50, No.5, 2026, DOI:10.32604/biocell.2026.075139 - 13 May 2026

    Abstract Objectives: Plant-derived bioactive molecules are increasingly recognized as valuable therapeutic resources for managing diverse pathological conditions, particularly those involving vascular inflammation. This study aimed to determine whether veratramine (VRT), a naturally occurring steroidal alkaloid found in Veratrum species of the Liliaceae family, attenuates LPS-induced vascular and pulmonary inflammation by upregulating heme oxygenase-1 (HO-1) and modulating the Nrf2, nuclear factor (NF)-κB, and signal transducer and activator of transcription (STAT1) signaling pathways. Methods: The study assessed the modulatory effects of VRT on HO-1, cyclooxygenase-2 (COX-2), and inducible nitric oxide synthase (iNOS) in LPS-activated human umbilical vein endothelial cells… More > Graphic Abstract

    Anti-Inflammatory Effects of Veratramine against Lipopolysaccharide-Induced Inflammation

  • Open Access

    REVIEW

    Role of Protein Misfolding in Human Kidney Diseases

    Sebastián Jaurreteche1,2,*, María Luana Brajkovic2, María Victoria Del Rosal2, Graciela Venera3, Carlos Daniel De la Vega Elena4

    BIOCELL, Vol.50, No.5, 2026, DOI:10.32604/biocell.2026.073790 - 13 May 2026

    Abstract Protein misfolding has emerged as a central mechanism in the pathogenesis of human kidney diseases. Normally, proteins achieve their native conformation through highly regulated folding processes in the endoplasmic reticulum (ER) and cytoplasm, assisted by molecular chaperones and quality-control pathways. However, genetic variants, environmental stressors, or cellular overload can destabilize this system, resulting in unfolded or misfolded proteins that trigger aggregation, amyloid formation, endoplasmic reticulum stress, and activation of the unfolded protein response (UPR). These events may ultimately lead to loss of function, gain of toxic function, and apoptosis. This review summarizes the structural basis… More >

  • Open Access

    REVIEW

    The Immune-Centric Revolution in the Treatment of Musculoskeletal Disease: Autologous PBMNC and PRP-PBMNC Enriched—A Narrative Review

    Andrea De Matthaeis1, Laura Rehak2,*, Maria Bianchi3, Rossana Putzulu3, Nicola Piccirillo3,4, Giulio Maccauro1

    BIOCELL, Vol.50, No.5, 2026, DOI:10.32604/biocell.2026.073783 - 13 May 2026

    Abstract For over two decades, mesenchymal stem cells (MSCs) have been recognised as the cornerstone of orthobiologic treatments for musculoskeletal diseases. However, clinical evidence increasingly indicates that MSC engraftment in inflamed tissues is minimal and transient, with effects mainly driven by paracrine and immunomodulatory mechanisms induced by macrophage efferocytosis. This evolving paradigm emphasises the immune system as the central orchestrator of tissue repair. Peripheral blood mononuclear cells (PBMNCs) have emerged as potent effectors of regenerative inflammation, mediating apoptotic cell clearance through efferocytosis, facilitating the transition of macrophages from pro-inflammatory (M1) to reparative (M2) phenotypes, and releasing… More >

  • 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

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