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Search Results (14)
  • Open Access

    REVIEW

    Melatonin as a Neuroprotective Agent in Ischemic Stroke: Mechanistic Insights Centralizing Mitochondria as a Potential Therapeutic Target

    Mayuri Shukla1, Soraya Boonmag2, Parichart Boontem1, Piyarat Govitrapong1,*

    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 >

  • Open Access

    ARTICLE

    CSRNP1 Promotes Apoptosis and Mitochondrial Dysfunction via ROS-Mediated JNK/p38 MAPK Pathway Activation in Hepatocellular Carcinoma

    Huihui Shi1,#, Lei Chen2,#, Juan Huang3,#, Xuejing Lin2, Lei Huang4, Min Tang4, Kai Lu5,*, Wenchao Wang4,*, Maoling Zhu1,§,*

    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

    <i>CSRNP1</i> Promotes Apoptosis and Mitochondrial Dysfunction via ROS-Mediated JNK/p38 MAPK Pathway Activation in Hepatocellular Carcinoma

  • Open Access

    REVIEW

    Endothelial and Mitochondrial Dysfunction in COPD Pathophysiology: Focus on Homocysteine–L-Carnitine Interplay

    Eduard Belskikh1,*, 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 >

  • Open Access

    REVIEW

    Drug-Induced Insulin Sensitivity Impairments: Potential Involvement of Disturbed Mitochondrial Dynamics and Mitophagy Pathways

    Mutamba Ropafadzo Peace1, Thobeka Madide1,2, Ntethelelo Sibiya1,*

    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 >

  • Open Access

    REVIEW

    Mitochondrial Dysfunction in Parkinson’s Disease: Is Impaired Deuterium Depleted Nutrient Supply by Gut Microbes a Primary Factor?

    Stephanie Seneff1,*, Greg Nigh2, Anthony M. Kyriakopoulos3,4

    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 >

  • Open Access

    REVIEW

    Crosstalk between mitochondrial dysfunction and benign prostatic hyperplasia: unraveling the intrinsic mechanisms

    Huan Liu1,#, Yan Li2,#, Jizhang Qiu1, Junchao Zhang1, Huan Lai1, Xinhua Zhang1,*

    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 >

  • Open Access

    ARTICLE

    ERRγ Promotes Multiple Myeloma Survival by Coordinating NF-κB Signaling and Mitochondrial Apoptosis Regulation

    Xiaobing Zhou1,#, Ying Li2,#, Zizi Jing1, Wei Yu1, Jianbin Chen1,*

    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

    ERRγ Promotes Multiple Myeloma Survival by Coordinating NF-κB Signaling and Mitochondrial Apoptosis Regulation

  • Open Access

    REVIEW

    Rotenone-Induced Mitochondrial Dysfunction, Neuroinflammation, Oxidative Stress, and Glial Activation in Parkinson’s and Alzheimer’s Diseases

    Carmen Rubio1,#, Norma Serrano-GarcíA1,#, Elisa Taddei1, Eduardo CastañEda2, HéCtor Romo1,3, MoiséS Rubio-Osornio4,*

    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 >

  • Open Access

    REVIEW

    The Crucial Role of NAD+ in Mitochondrial Metabolic Regulation

    Kumudesh Mishra1,2,*, Or Kakhlon1,2

    BIOCELL, Vol.49, No.7, pp. 1101-1123, 2025, DOI:10.32604/biocell.2025.061725 - 25 July 2025

    Abstract Mitochondria are central organelles in cellular metabolism, orchestrating energy production, biosynthetic pathways, and signaling networks. Nicotinamide adenine dinucleotide (NAD+) and its reduced form (NADH) are essential for mitochondrial metabolism, functioning both as redox coenzymes and as signaling agents that help regulate cellular balance. Thus, while its major role is in energy production, NAD+ is widely recognized as a metabolic cofactor and also serves as a substrate for various enzymes involved in cellular signaling, like sirtuins (SIRTs), poly (ADP-ribosyl) polymerases (PARPs), mono (ADP-ribosyl) transferases, and CD38. Sirtuins, a family of NAD+-dependent deacetylases, are critical in this regulatory network.… More >

  • Open Access

    ARTICLE

    Nigericin-induced apoptosis in acute myeloid leukemia via mitochondrial dysfunction and oxidative stress

    BHAVYADHARSHINI ARUN1,#, PRARTHANA GOPINATH1,2,#, ANUP JHA1,3, NISHTHA TRIPATHI1, SYED G DASTAGER4,*, SYED K HASAN1,3,*

    Oncology Research, Vol.33, No.8, pp. 2161-2174, 2025, DOI:10.32604/or.2025.062951 - 18 July 2025

    Abstract Background: Acute Myeloid Leukemia (AML) is a highly aggressive clonal hematological malignancy with limited treatment options. This study aimed to evaluate the therapeutic potential of nigericin, a polyether ionophore derived from Streptomyces DASNCL-29, as a mitochondrial-targeted agent for AML treatment. Methods: Nigericin was isolated from Streptomyces DASNCL-29 and characterized via chromatography and NMR. Its cytotoxicity was tested in MOLM13 (sensitive and venetoclax-resistant) and HL60 (sensitive and cytarabine-resistant) cells using the MTT assay. Mitochondrial dysfunction was assessed by measuring reactive oxygen species (ROS), mitochondrial membrane potential (Δψm), and mitochondrial mass. Apoptosis was evaluated with Annexin V/PI assays… More > Graphic Abstract

    Nigericin-induced apoptosis in acute myeloid leukemia via mitochondrial dysfunction and oxidative stress

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