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REVIEW

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
（This article belongs to the Special Issue: Homeostasis of Mitochondria: Unraveling its Multifaceted Role in Health and Disease)
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 >

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1849

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Desirée Victoria-Montesinos^*, Pablo Barcina-Pérez^*, Ana María García-Muñoz
BIOCELL, Vol.50, No.6, 2026, DOI:10.32604/biocell.2026.077286 - 09 June 2026
（This article belongs to the Special Issue: MitoROS: Exploring Mitochondria and Oxidative Stress)
Abstract Mitochondrial dysfunction is a central hallmark of metabolic, hepatic, cardiovascular, and neurodegenerative diseases. Dietary polyphenols modulate mitochondrial pathways, but their integrated effects remain poorly appreciated. This narrative review synthesizes preclinical and clinical evidence on four polyphenols (resveratrol, epigallocatechin-3-gallate, quercetin, and oleuropein) and examines their mechanisms in mitochondrial biogenesis, mtDNA protection, and mitophagy. Experimental studies indicate that these compounds activate conserved adaptive pathways, including sirtuin 1 (SIRT1) and peroxisome proliferator-activated receptor gamma coactivator 1 alpha (PGC-1α), AMP-activated protein kinase (AMPK), and PTEN-induced kinase 1 (PINK1) with Parkin, therapy enhancing mitochondrial biogenesis, reducing oxidative stress, and promoting More >

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459

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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
（This article belongs to the Special Issue: Melatonin and Mitochondria: Exploring New Frontiers)
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 >

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459

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REVIEW

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
（This article belongs to the Special Issue: Natural and Synthetic Small Molecules in the Regulation of Immune Cell Functions)
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 >

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554

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REVIEW

Jernej Jorgačevski^1,2, Maja Potokar^1,2,*
BIOCELL, Vol.50, No.6, 2026, DOI:10.32604/biocell.2026.077871 - 09 June 2026
（This article belongs to the Special Issue: Transporters and Channels in Brain Physiology: From Molecular Biophysics to Cellular Dynamics)
Abstract Astrocytes contribute to central nervous system (CNS) homeostasis by taking up and releasing various transmitters, ions, water, and energy molecules, thereby modulating neuronal function and maintaining the blood-brain barrier. The dynamic delivery, retrieval, and recycling of transporters, channels, receptors, and vesicular cargo at the astrocyte plasma membrane are regulated by the cytoskeleton networks composed of microtubules, actin filaments, and intermediate filaments. Increasing evidence indicates that changes in vesicle trafficking disrupt astrocyte–neuron communication and contribute to CNS dysfunction in pathological conditions. This review presents recent findings on vesicle trafficking in astrocytes with emphasis on the cytoskeletal More >

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484

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ARTICLE

Guoxu Ma, Yonglu Huang, Fan Gong, Jianke Wu, Yi Ding, Ziyang Zhang, Xiaoliang Li, Jian Gao, Tingting Dang, Bowen Zhang^*
BIOCELL, Vol.50, No.6, 2026, DOI:10.32604/biocell.2026.078402 - 09 June 2026
（This article belongs to the Special Issue: Bioactive Natural Components as Regulators of Cellular Pathways and Disease Progression)
Abstract Objectives: Sciatic nerve injury (SNI) impairs quality of life, and Lycium barbarum polysaccharides (LBP) may exert therapeutic effects via regulating Schwann cell (SC) mitochondrial stability, though the mechanism remains unclear. The study aimed to elucidate the therapeutic mechanisms of LBP in mitigating sciatic nerve injury by protecting Schwann cells via the estrogen receptor 1 (ESR1)/thioredoxin 2 (Trx2) pathway. Methods: An in vitro SNI model was established by inducing RSC96 cells with H₂O₂. Cell counting kit-8 (CCK8) assay, enzyme-linked immunosorbent assay (ELISA), Western blot, reactive oxygen species (ROS) and adenosine triphosphate (ATP) quantification, and mitochondrial membrane potential (MMP) detection were… More >

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413

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Junming Yan, Boran Xiong, Yingjie Zhu^*
BIOCELL, Vol.50, No.6, 2026, DOI:10.32604/biocell.2026.075319 - 09 June 2026
（This article belongs to the Special Issue: Homeostasis of Mitochondria: Unraveling its Multifaceted Role in Health and Disease)
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 >

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383

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Bohan Lin^#, Wei Liu^#, Xiu Ni, Fuyi Shen^*
BIOCELL, Vol.50, No.6, 2026, DOI:10.32604/biocell.2026.077413 - 09 June 2026
Abstract Background: Postoperative cognitive dysfunction (POCD) is a common neurological complication in elderly patients. However, the mechanism by which glutamate ionotropic receptor NMDA type subunit 2B (GluN2B) contributes to POCD development remains incompletely understood. This study aimed to investigate the effects of GluN2B overexpression on POCD improvement and elucidate its underlying molecular mechanisms. Methods: In vitro, lipopolysaccharide (LPS) was used to induce inflammation in mouse primary microglia, and a microglia-HT22 neuron co-culture system was established to simulate the neurotoxic environment. Overexpression and knockdown constructs for GluN2B and brain-derived neurotrophic factor (BDNF) were generated. Western blot, ELISA, immunofluorescence, and… More >

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379

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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 >

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326

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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 >

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476