Moo Hyun Kim¹, Yongdae Yoon², Chang Wan Kim¹, Jun-Won Lee³, Bhupendra Regmi², Saher Fatima², Moon Young Kim^2,3, Soon Koo Baik^2,3, Pil Young Jung^1,*, Young Woo Eom^2,*

BIOCELL, Vol.50, No.6, 2026, DOI:10.32604/biocell.2026.076364 - 09 June 2026

Abstract Background: Although transforming growth factor-β (TGF-β) drives hepatic stellate cell activation and fibrogenesis, the mechanisms by which 12-O-tetradecanoylphorbol-13-acetate (TPA) modulates these processes in TGF-β1-activated hepatic stellate cells remain to be determined. Therefore, we investigated whether TPA alleviates fibrosis in TGF-β1-treated hepatic stellate cells and regulates both canonical and non-canonical pathways. Further, we assessed whether inhibitors of these pathways similarly affect proliferation and fibrosis in LX-2 cells. Methods: LX-2 hepatic stellate cells were used as the experimental model. Cells were treated with TPA, TGF-β, or TGF-β plus TPA, and Yes-associated protein (YAP) and protein kinase B (PKB;… More >

Weina Xu¹, Yi Xia¹, Qing Shen¹, Ling Ai¹, Yingye Lu^2,*

BIOCELL, Vol.50, No.6, 2026, DOI:10.32604/biocell.2026.076001 - 09 June 2026

Abstract Background: Dysfunction of decidual macrophages (dMφ) mediated by high mobility group box 1 (HMGB1) is related to unexplained recurrent spontaneous abortion (URSA), but its upstream regulatory mechanism remains unclear. The research explores whether miR-216a-5p regulates the toll-like receptor 4/nuclear factor-κB/nucleotide-binding oligomerization domain-like receptor protein 3 (TLR4/NF-κB/NLRP3) signaling axis by targeting HMGB1, thereby affecting the M1 polarization and pyroptosis of dMφ in URSA. Methods: The URSA mouse model was established, and primary dMφ was isolated and cultured. HMGB1 and miR-216a-5p were overexpressed or knocked down. Their expressions were examined. Their targeting relationship was verified through a bioinformatics… More > Graphic Abstract

Debasish Bandyopadhyay^1,*, Romit Majumder^1,2,#, Madhuri Datta^1,2,#, Adrita Banerjee^1,2, Aindrila Chattopadhyay²

BIOCELL, Vol.50, No.6, 2026, DOI:10.32604/biocell.2026.075963 - 09 June 2026

Abstract Non-steroidal anti-inflammatory drugs (NSAIDs) are widely prescribed, but their long-term use frequently results in gastric mucosal injury. Emerging evidence indicates that, beyond cyclooxygenase inhibition, mitochondrial dysfunction represents a central mechanism driving NSAID-induced gastric epithelial damage. This review aims to critically synthesize current evidence on mitochondria-centered pathways involved in NSAID-induced gastric ulceration and to evaluate the therapeutic relevance of melatonin in this context. We highlight how NSAIDs impair mitochondrial bioenergetics, promote excessive reactive oxygen species generation, disrupt membrane potential, and activate apoptotic signaling, thereby compromising mucosal integrity. Importantly, melatonin exerts multifaceted gastroprotective actions by preserving mitochondrial More >

Xing-Guo Li^1,2,3,#, Lu-Kai Wang^4,#, Fu-Ming Tsai⁵, Hsueh-Chun Wang^1,*

BIOCELL, Vol.50, No.6, 2026, DOI:10.32604/biocell.2026.075492 - 09 June 2026

Abstract Itaconate, produced by aconitate decarboxylase 1 (ACOD1, also known as IRG1), acts as a key immunometabolite that inhibits succinate dehydrogenase (SDH) and can engage reduction-oxidation (redox)-sensitive signaling programs. This review summarizes the emerging, context-dependent roles of the ACOD1-itaconate axis in cancer, while critically distinguishing between the effects of endogenous itaconate and its cell-permeable derivatives. In tumor cells, endogenous ACOD1 expression or uptake via solute carrier family 13 member 3 (SLC13A3) alters oxidative phosphorylation and glycolysis. In the tumor microenvironment, myeloid-derived itaconate contributes to immune tolerance by reducing dendritic-cell cross-priming and limiting CD8⁺ T-cell metabolic activity. Moreover, More >

Junming Yan, Boran Xiong, Yingjie Zhu^*

BIOCELL, Vol.50, No.6, 2026, DOI:10.32604/biocell.2026.075319 - 09 June 2026

Abstract Objective: Neural stem cells (NSCs) are essential for replenishing nerve cells, providing neuroprotection, and repairing damaged brain function, while mitophagy is critical for maintaining NSCs’ homeostasis. The study investigated whether pyruvate kinase M2 (PKM2) regulates NSCs’ proliferation and differentiation by modulating mitophagy. Method: This study established a model of excessive autophagy in neural stem cell mitochondria induced by cobalt chloride (CoCl₂) and used plasmid transfection technology to knock down PKM2 expression, examining its effects on NSCs proliferation and differentiation. Additionally, potential mechanisms were explored by overexpressing phosphatase and tensin homolog-induced putative kinase 1 (PINK1) and adding the… More > Graphic Abstract

Andrew Scarborough¹, Yvoni Kyriakidou¹, Derek C. Lee², Tomás Duraj², Thomas N. Seyfried², Isabella D. Cooper^1,*

BIOCELL, Vol.50, No.6, 2026, DOI:10.32604/biocell.2026.074152 - 09 June 2026

Abstract The global rise in chronic, non-communicable diseases (NCDs) is inextricably linked to metabolic dysfunction, with hyperinsulinaemia acting as a potent upstream driver of ageing and age-related disease. Some of the most burdensome diseases of our time, including type 2 diabetes, cardiovascular disease, cancer, and neurodegenerative conditions, such as Alzheimer’s disease (AD), are largely underpinned by insulin resistance as part of a broader system of metabolic and mitochondrial dysfunction. These pathologies are particularly pronounced in the developed world, where obesity and other lifestyle-related conditions are major contributors to disease burden and premature mortality. As an upstream… More >

Xuechun Liao^1,#, Xiaoxiao Chen^2,#, Shulan Wei¹, Qiong Li¹, Yanqin Zhao¹, Yuying Xiao¹, Qi Zhou¹, Jianping Chen^1,*, Jinlei He^1,*

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

Zhiye Zhou^1,2, Jianan Chen³, Qiang Zhu^3,*

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

Yingjian Wang¹, Chen Jin¹, Yixue Qin¹, Xinghong Yao², Ye Zeng^1,*

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 >

Ralf Weiskirchen¹, Amedeo Lonardo^2,*

BIOCELL, Vol.50, No.5, 2026, DOI:10.32604/biocell.2026.076177 - 13 May 2026

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