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 >

Hailong Li^1,#, Wen Ouyang^2,#, Yiyin Long¹, Yun Peng¹, Ziyi Liu¹, Qi Zhou¹, Rong Xu^1,*, Wei Du^1,*

Oncology Research, Vol.33, No.9, pp. 2549-2571, 2025, DOI:10.32604/or.2025.065050 - 28 August 2025

Abstract Background: The study aimed to explore the clinical value of mitochondrial ribosomal protein L18 (MRPL18) in breast cancer. Methods: Multiple databases were used to validate the expression of MRPL18. The prognostic impact and predictive value of MRPL18 were evaluated by using predictive models. Protein-protein interaction (PPI) networks were constructed by using GeneMANIA. Enrichment analysis is used to explore the signaling pathway regulated by MRPL18. Cell counting kit-8 (CCK-8) assays, colony formation, migration assays, flow cytometry, and xenograft models were employed to evaluate the role of MRPL18 in tumor progression. The immune response of MRPL18 was More >

Xiaobing Zhou^1,#, Ying Li^2,#, Zizi Jing¹, Wei Yu¹, Jianbin Chen^1,*

Oncology Research, Vol.33, No.9, pp. 2399-2420, 2025, DOI:10.32604/or.2025.063700 - 28 August 2025

Abstract Background: Multiple myeloma (MM) remains a formidable clinical challenge due to its high relapse rate and resistance to existing therapies. Estrogen-related receptor gamma (ERRγ), a nuclear receptor critical for cellular energy metabolism, has been implicated in various cancers. but its role in MM remains unclear. Methods: ERRγ expression was assessed using bioinformatics and RT-qPCR. Functional studies were conducted through siRNA-mediated ERRγ knockdown and treatment with the inverse agonist GSK5182 to examine their effects on MM cell proliferation and apoptosis. Results: ERRγ was significantly upregulated in the bone marrow of MM patients, correlating with advanced clinical stages… More > Graphic Abstract

Carmen Rubio^1,#, Norma Serrano-GarcíA^1,#, Elisa Taddei¹, Eduardo CastañEda², HéCtor Romo^1,3, MoiséS Rubio-Osornio^4,*

BIOCELL, Vol.49, No.8, pp. 1391-1412, 2025, DOI:10.32604/biocell.2025.066320 - 29 August 2025

Abstract Rotenone is a lipophilic herbicide extensively utilized in experimental neurodegenerative models because of its capacity to disrupt complex I of the mitochondrial electron transport chain. This inhibition results in reduced ATP synthesis, elevated reactive oxygen species (ROS) formation, and mitochondrial malfunction, which instigates oxidative stress and cellular damage, critical elements in neurodegenerative disorders like Parkinson’s disease (PD), amyotrophic lateral sclerosis (ALS), and Alzheimer’s disease (AD). In addition to causing direct neuronal injury, rotenone significantly contributes to the activation of glial cells, specifically microglia and astrocytes. Activated microglia assumes a proinflammatory (M1) phenotype, distinguished by the… More >