Zongmeng Zhang^1,2,#, Cai Chen^3,#, Shaorui Rui³, Conghan Li³, Jiong Gu^3,*, Liang He^3,*

BIOCELL, Vol.50, No.1, 2026, DOI:10.32604/biocell.2025.073085 - 23 January 2026

Abstract Objective: Hepatocellular carcinoma (HCC) ranks among the most prevalent malignant tumors globally. Metabolically associated fatty liver disease is a significant risk factor for HCC. Adiponectin, a key regulatory protein in glucolipid metabolism, presents potential as an anti-tumor target in HCC cells. The study focused on evaluating the anti-HCC properties of AdipoRon, an agonist of the adiponectin receptor. Method: Cell viability and proliferation were assessed using the cell counting kit-8 and colony formation assays, respectively. AdipoRon’s effect on HCC cell damage was evaluated via flow cytometry, apoptosis, and (lactate dehydrogenase) LDH assays. Mitochondrial function was evaluated… More >

Mayuri Shukla¹, Soraya Boonmag², Parichart Boontem¹, Piyarat Govitrapong^1,*

BIOCELL, Vol.50, No.1, 2026, DOI:10.32604/biocell.2025.072557 - 23 January 2026

Abstract Ischemic stroke is one of the major causes of long-term disability and mortality worldwide. It results from an interruption in the cerebral blood flow, triggering a cascade of detrimental events like oxidative stress, mitochondrial dysfunction, neuroinflammation, excitotoxicity, and apoptosis, causing neuronal injury and cellular death. Melatonin, a pleiotropic indoleamine produced by the pineal gland, has multifaceted neuroprotective effects on stroke pathophysiology. Interestingly, the serum melatonin levels are associated with peroxidation and antioxidant status, along with mortality score in patients with severe middle cerebral artery infarction. Melatonin exhibits strong antioxidant, anti-inflammatory, and anti-apoptotic properties and preserves More >

Wei-Ting Hsueh^1,#, Kwang-Yu Chang^1,2,3,#, Chin-Chuan Tsai^4,5, Kuan-Tso Chen^5,6, Kuen-Jang Tsai⁷, Zi-Xuan Hong⁸, Chan-Chuan Liu², Jui-Mei Chu², Li-Ying Qiu², Yu-Yan Lan⁸, Chia-Hung Chien^8,*

Oncology Research, Vol.34, No.2, 2026, DOI:10.32604/or.2025.071258 - 19 January 2026

Abstract Objectives: Glioblastoma (GBM) is a prevalent malignant brain tumor prone to drug resistance. We previously found a strong correlation between SH3 domain GRB2-like endophilin B1 (SH3GLB1) and superoxide dismutase 2 (SOD2), which converts O₂ to hydrogen peroxide (H₂O₂). Prior studies show that H₂O₂ redox signaling is vital for physiological processes and can drive tumor progression. Therefore, we aim to define how H₂O₂ signaling regulates SH3GLB1 and AKT (protein kinase B) pathways in GBM and to assess whether modulating H₂O₂ reverses temozolomide (TMZ) resistance. Methods: We used cultured cells and pharmacological inhibitors and activators to confirm the significance of… More > Graphic Abstract

Huihui Shi^1,#, Lei Chen^2,#, Juan Huang^3,#, Xuejing Lin², Lei Huang⁴, Min Tang⁴, Kai Lu^5,*, Wenchao Wang^4,*, Maoling Zhu^1,§,*

Oncology Research, Vol.34, No.1, 2026, DOI:10.32604/or.2025.068737 - 30 December 2025

Abstract Background: Hepatocellular carcinoma (HCC) is one of the leading causes of cancer-related mortality worldwide. This study aimed to identify key genes involved in HCC development and elucidate their molecular mechanisms, with a particular focus on mitochondrial function and apoptosis. Methods: Differential expression analyses were performed across three datasets—The Cancer Genome Atlas (TCGA)-Liver Hepatocellular Carcinoma (LIHC), GSE36076, and GSE95698—to identify overlapping differentially expressed genes (DEGs). A prognostic risk model was then constructed. Cysteine/serine-rich nuclear protein 1 (CSRNP1) expression levels in HCC cell lines were assessed via western blot (WB) and quantitative reverse transcription polymerase chain reaction (qRT-PCR).… More > Graphic Abstract

Virna Margarita Martín Giménez¹, SebastiáN GarcíA MenéNdez^2,3, Luiz Gustavo A. Chuffa⁴, Vinicius Augusto SimãO⁴, Russel J. Reiter⁵, Ramaswamy Sharma⁶, Walter Balduini⁷, Carla Gentile⁸, Walter Manucha^2,3,*

BIOCELL, Vol.49, No.12, pp. 2245-2282, 2025, DOI:10.32604/biocell.2025.071830 - 24 December 2025

Abstract Neurodegenerative diseases (NDs) such as Alzheimer’s disease (AD), Parkinson’s disease (PD), Huntington’s disease (HD), and amyotrophic lateral sclerosis (ALS) are characterized by progressive neuronal loss, which is closely linked to mitochondrial dysfunction. These pathologies involve a complex interplay of genetics, protein misfolding, and cellular stress, culminating in impaired energy metabolism, an increase in reactive oxygen species (ROS), and defective mitochondrial quality control. The accumulation of damaged mitochondria and dysregulation of pathways such as the Integrated Stress Response (ISR) are central to the pathogenesis of these conditions. This review explores the critical relationship between mitochondrial stress… More >

Eduard Belskikh^1,*, Yuliya Marsyanova², Denis Melnikov³, Oleg Uryasev¹, Valentina Zvyagina²

BIOCELL, Vol.49, No.11, pp. 2093-2123, 2025, DOI:10.32604/biocell.2025.069272 - 24 November 2025

Abstract Elevated homocysteine is a clinically relevant metabolic signal in chronic obstructive pulmonary disease (COPD). Higher circulating levels track with oxidative stress, endothelial dysfunction, mitochondrial impairment, and pulmonary vascular remodeling, rise with disease severity, and may contribute to the excess cardiovascular risk—although effect sizes and causality remain uncertain. This review centers on the homocysteine–carnitine relationship in COPD pathophysiology. Carnitine deficiency, prevalent in COPD, can worsen mitochondrial bioenergetics, promote accumulation of acyl intermediates, and reduce nitric oxide bioavailability via endothelial nitric oxide synthase uncoupling (eNOS). Conversely, restoring carnitine status in experimental and early clinical settings has been… More >

Mutamba Ropafadzo Peace¹, Thobeka Madide^1,2, Ntethelelo Sibiya^1,*

BIOCELL, Vol.49, No.11, pp. 2069-2091, 2025, DOI:10.32604/biocell.2025.068017 - 24 November 2025

Abstract The pathogenesis of insulin resistance is influenced by environmental factors, genetic predispositions, and several medications. Various drugs used to manage multiple ailments have been shown to induce insulin resistance, which could lead to Type II Diabetes mellitus (T2DM). Central to drug-induced insulin resistance is mitochondrial dysfunction. Amongst disturbed pathways in drug-induced mitochondrial toxicity is mitophagy, a process that removes dysfunctional mitochondria through the lysosomal pathways to maintain mitochondrial quality. A balance must always be maintained between mitochondrial dynamics and mitophagy, as any alterations may contribute to the pathogenesis of metabolic diseases such as diabetes mellitus.… More >

Russel J. Reiter^1,*, Ramaswamy Sharma^2,*, Walter Manucha³, Walter Balduini⁴, Doris Loh⁵, Demetrios A. Spandidos⁶, Alejandro Romero⁷, Vasiliki E. Georgakopoulou⁸, Wei Zhu⁹

BIOCELL, Vol.49, No.11, pp. 2033-2067, 2025, DOI:10.32604/biocell.2025.067661 - 24 November 2025

Abstract The development of cancer cell resistance to conventional treatments continues to be a major obstacle in the successful treatment of tumors of many types. The discovery of a highly efficient direct and indirect free radical scavenger, melatonin, in the mitochondrial matrix may be a factor in determining both the occurrence of cancer cell drug insensitivity as well as radioresistance. This relates to two of the known hallmarks of cancer, i.e., exaggerated free radical generation in the mitochondria and the development of Warburg type metabolism (glycolysis). The hypothesis elaborated in this report assumes that the high… More >

Stephanie Seneff^1,*, Greg Nigh², Anthony M. Kyriakopoulos^3,4

BIOCELL, Vol.49, No.9, pp. 1545-1572, 2025, DOI:10.32604/biocell.2025.066687 - 25 September 2025

Abstract Deuterium is a heavy isotope of hydrogen, with an extra neutron, endowing it with unique biophysical and biochemical properties compared to hydrogen. The ATPase pumps in the mitochondria depend upon proton motive force to catalyze the reaction that produces ATP. Deuterons disrupt the pumps, inducing excessive reactive oxygen species and decreased ATP synthesis. The aim of this review is to develop a theory that mitochondrial dysfunction due to deuterium overload, systemically, is a primary cause of Parkinson’s disease (PD). The gut microbes supply deuterium-depleted short chain fatty acids (SCFAs) to the colonocytes, particularly butyrate, and… More >

Huan Liu^1,#, Yan Li^2,#, Jizhang Qiu¹, Junchao Zhang¹, Huan Lai¹, Xinhua Zhang^1,*

Canadian Journal of Urology, Vol.32, No.4, pp. 255-269, 2025, DOI:10.32604/cju.2025.066523 - 29 August 2025

Abstract Benign prostatic hyperplasia (BPH) represents a prevalent etiology of lower urinary tract symptoms (LUTS) in the male population, clinically defined by a non-malignant proliferation of prostatic tissue. While BPH exhibits a high prevalence among older male populations globally, the precise underlying mechanisms contributing to its development remain incompletely elucidated. Mitochondria, essential organelles within eukaryotic cells, are critical for cellular bioenergetics, the regulation of reactive oxygen species (ROS) generation, and the modulation of cell death pathways. The maintenance of mitochondrial homeostasis involves a complex interplay of processes. By synthesizing previous literature, this review discusses mitochondrial homeostasis More >