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): 2024 Impact Factor 1.0; Journal Citation Report/Science Edition (JCR); Scopus; Scopus Citescore (Impact per Publication 2024): 2.0; SNIP (Source Normalized Impact per Paper 2024): 0.256; Sociedad Argentina de Investigaciones en Bioquímica y Biología Molecular (SAIB); Portico, etc.
Open Access
REVIEW
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
Open Access
REVIEW
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 >
Open Access
REVIEW
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 >
Open Access
REVIEW
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
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 >
Open Access
ARTICLE
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
Open Access
ARTICLE
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
ARTICLE
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
Open Access
ARTICLE
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
Open Access
ARTICLE
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 >
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