Submit

Login Login

Register Register

Home / Journals / BIOCELL / Vol.50, No.5, 2026
Journal Menu
Special Issues
Table of Content

All issues

Online First

2026

2025

2024

2023

2022

2021

2020

2019

2018

2017

2016

2015

2014

2013

2012

2011

2010

2009

2008

2007

2006

2005

2004

2003

2002

SAIB Annual Meetings

cover

On the Cover

Obesity significantly influences liver health by promoting the onset and progression of metabolic dysfunction-associated steatotic liver disease (MASLD). Hepatocellular carcinoma (HCC), the most prevalent form of liver cancer, is increasingly associated with MASLD through intricate genetic and molecular mechanisms. Obesity-induced MASLD entails alterations in hepatocytes resulting from lipid accumulation, oxidative stress, inflammation, and dysregulated signaling pathways such as mTOR, AMPK, and NF-κB. These factors impact cellular processes including growth, apoptosis, autophagy, migration, immune response, angiogenesis, and differentiation. Optimal management of MASLD-HCC depends on comprehensive risk evaluation, timely diagnosis, and the implementation of advanced therapeutic approaches. The cover image was created, in part, with AI-generated content via Copilot which was further modified using copyrighted elements by Servier Medical Art (SMART), licensed under the Creative Commons Attribution 4.0 International License (CC BY 4.0).

View this paper

Show export options

  • Open AccessOpen Access

    REVIEW

    Obesity, Metabolic Dysfunction-Associated Steatotic Liver Disease and Hepatocellular Carcinoma: How Molecular Changes Impact Cellular Functions

    Ralf Weiskirchen1, Amedeo Lonardo2,*
    BIOCELL, Vol.50, No.5, 2026, DOI:10.32604/biocell.2026.076177 - 13 May 2026
    （This article belongs to the Special Issue: Molecular Insights into the Obesity-Cancer Nexus: From Cellular Mechanisms to Therapeutic Targets)
    Abstract Obesity is a complex chronic condition characterized by an excess of body fat that manifests in various clinical pathophenotypes, each affecting liver health differently. One significant cause of chronic liver diseases among those living with obesity is metabolic dysfunction-associated steatotic liver disease (MASLD), which is linked to one or more cardiometabolic risk factors in individuals who do not engage in harmful alcohol consumption. Hepatocellular carcinoma (HCC) is the most common form of primary liver cancer and is increasingly being associated with MASLD through intricate immunological, cellular, proinflammatory, molecular, and genetic mechanisms. In this review, we More >

    Graphic Abstract

    Obesity, Metabolic Dysfunction-Associated Steatotic Liver Disease and Hepatocellular Carcinoma: How Molecular Changes Impact Cellular Functions

    View

    900

    Download

    372

  • Open AccessOpen Access

    REVIEW

    AKR1B1 as A Metabolic Enzyme and Pleiotropic Signaling Hub

    Yingjian Wang1, Chen Jin1, Yixue Qin1, Xinghong Yao2, Ye Zeng1,*
    BIOCELL, Vol.50, No.5, 2026, DOI:10.32604/biocell.2026.076298 - 13 May 2026
    Abstract Aldo-keto reductase family 1 member B1 (AKR1B1) was historically characterized as the first and generally rate-limiting enzyme of the polyol pathway and, consequently, was primarily implicated in the pathogenesis of diabetic complications. Recent advances, however, have repositioned AKR1B1 as a pleiotropic signaling hub whose biological functions extend far beyond glucose metabolism. This review systematically integrates the complex regulatory network governing AKR1B1, including transcriptional control by tumor protein p53 (p53) and nuclear factor erythroid 2-related factor 2 (Nrf2), and its dual functionality as both a metabolic enzyme and a non-catalytic signaling scaffold. We elucidate its role More >

    View

    1217

    Download

    548

  • Open AccessOpen 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
    （This article belongs to the Special Issue: Tissue Regeneration and Vascularization: From Stem Cells to Functional Tissues)
    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 >

    View

    1226

    Download

    449

  • Open AccessOpen 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 >

    View

    1433

    Download

    670

  • Open AccessOpen 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
    （This article belongs to the Special Issue: Novel Targeted Therapy in Oncology)
    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 >

    View

    1055

    Download

    444

  • Open AccessOpen 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
    （This article belongs to the Special Issue: Bioactive Natural Components as Regulators of Cellular Pathways and Disease Progression)
    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

    View

    1036

    Download

    368

  • Open AccessOpen 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 >

    View

    963

    Download

    393

  • Open AccessOpen 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

    View

    897

    Download

    334

  • Open AccessOpen Access

    ARTICLE

    PD-1 Blockade Reduces Parasite Load and Restores Anti-Parasitic Immunity in Murine Visceral Leishmaniasis

    Xuechun Liao1,#, Xiaoxiao Chen2,#, Shulan Wei1, Qiong Li1, Yanqin Zhao1, Yuying Xiao1, Qi Zhou1, Jianping Chen1,*, Jinlei He1,*
    BIOCELL, Vol.50, No.5, 2026, DOI:10.32604/biocell.2026.077240 - 13 May 2026
    Abstract Objective: Immune checkpoint blockade holds therapeutic potential in visceral leishmaniasis; its underlying mechanism remains unclear. This study aimed to investigate the therapeutic potential and underlying immune mechanisms of Programmed cell death protein 1 (PD-1) blockade in experimental visceral leishmaniasis. Methods: BALB/c mice infected with Leishmania donovani received anti-PD-1 antibody at 35–44 days post-infection. Parasite burden in target organs, serum antibodies, hepatopathology, and transcriptome of the liver were analyzed. T cell exhaustion, activation, apoptosis, and inflammation genes were quantified in target organs. Results: PD-1 blockade reduced splenic parasite load (reduction rate = 82.6%, ***p < 0.001), enhanced hepatic granulomatous… More >

    Graphic Abstract

    PD-1 Blockade Reduces Parasite Load and Restores Anti-Parasitic Immunity in Murine Visceral Leishmaniasis

    View

    822

    Download

    306

  • Open AccessOpen Access

    ARTICLE

    Dioscin Regulates Mitochondrial Autophagy and Cell Cycle to Promote Pulpal Stem Cell Differentiation and Mineralization

    Zhiye Zhou1,2, Jianan Chen3, Qiang Zhu3,*
    BIOCELL, Vol.50, No.5, 2026, DOI:10.32604/biocell.2026.076758 - 13 May 2026
    Abstract Background: Human dental pulp stem cells (hDPSCs) are promising for dental tissue regeneration. Dioscin (Dio), a natural compound, has various biological activities, but its effects on hDPSCs are unclear. This study aims to systematically elucidate the effects of Dio on promoting the osteogenic differentiation of hDPSCs and the underlying molecular mechanisms. Methods: Characterized hDPSCs were treated with Dio. Cell viability, proliferation, osteogenic differentiation (alkaline phosphatase (ALP) activity, Alizarin Red S (ARS)), and migration (Transwell) were assessed. Mitophagy (fluorescence, Western blot for PTEN-induced kinase 1 (PINK1), parkin RBR E3 ubiquitin-protein ligase (PRKN), microtubule-associated protein 1 light chain… More >

    Graphic Abstract

    Dioscin Regulates Mitochondrial Autophagy and Cell Cycle to Promote Pulpal Stem Cell Differentiation and Mineralization

    View

    840

    Download

    321

Per Page:
Copyright© 2026 Tech Science Press
© 1997-2026 TSP (Henderson, USA) unless otherwise stated

Share Link