Mitochondrion最新文献_第9页

Mitochondria-targeted nanotherapeutics: A new frontier in neurodegenerative disease treatment 线粒体靶向纳米疗法：神经退行性疾病治疗的新前沿。

IF 3.9 3区生物学

Mitochondrion Pub Date : 2025-03-01 Epub Date: 2024-12-09 DOI: 10.1016/j.mito.2024.102000

Nishad Keethedeth, Rajesh Anantha Shenoi

{"title":"Mitochondria-targeted nanotherapeutics: A new frontier in neurodegenerative disease treatment","authors":"Nishad Keethedeth, Rajesh Anantha Shenoi","doi":"10.1016/j.mito.2024.102000","DOIUrl":"10.1016/j.mito.2024.102000","url":null,"abstract":"<div><div>Mitochondria are the seat of cellular energy and play key roles in regulating several cellular processes such as oxidative phosphorylation, respiration, calcium homeostasis and apoptotic pathways. Mitochondrial dysfunction results in error in oxidative phosphorylation, redox imbalance, mitochondrial DNA mutations, and disturbances in mitochondrial dynamics, all of which can lead to several metabolic and degenerative diseases. A plethora of studies have provided evidence for the involvement of mitochondrial dysfunction in the pathogenesis of neurodegenerative diseases such as Parkinson’s disease, Alzheimer’s disease, Huntington’s disease, and amyotrophic lateral sclerosis. Hence mitochondria have been used as possible therapeutic targets in the regulation of neurodegenerative diseases. However, the double membranous structure of mitochondria poses an additional barrier to most drugs even if they are able to cross the plasma membrane. Most of the drugs acting on mitochondria also required very high doses to exhibit the desired mitochondrial accumulation and therapeutic effect which in-turn result in toxic effects. Mitochondrial targeting has been improved by direct conjugation of drugs to mitochondriotropic molecules like dequalinium (DQA) and triphenyl phosphonium (TPP) cations. But being cationic in nature, these molecules also exhibit toxicity at higher doses. In order to further improve the mitochondrial localization with minimal toxicity, TPP was conjugated with various nanomaterials like liposomes. inorganic nanoparticles, polymeric nanoparticles, micelles and dendrimers. This review provides an overview of the role of mitochondrial dysfunction in neurodegenerative diseases and various nanotherapeutic strategies for efficient targeting of mitochondria-acting drugs in these diseases.</div></div>","PeriodicalId":18606,"journal":{"name":"Mitochondrion","volume":"81 ","pages":"Article 102000"},"PeriodicalIF":3.9,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142813853","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Endurance swimming exacerbates mitochondrial myopathy in mice with high mtDNA deletions 耐力游泳加剧线粒体肌病小鼠高mtDNA缺失。

IF 3.9 3区生物学

Mitochondrion Pub Date : 2025-03-01 Epub Date: 2025-02-14 DOI: 10.1016/j.mito.2025.102010

Sho Hanada , Kaori Ishikawa , Takanaga Shirai , Tohru Takemasa , Kazuto Nakada

引用次数: 0

Sex-dependent adaptations in heart mitochondria from transgenic mice overexpressing cytochrome b5 reductase-3 过表达细胞色素b5还原酶-3的转基因小鼠心脏线粒体的性别依赖性适应。

IF 3.9 3区生物学

Mitochondrion Pub Date : 2025-03-01 Epub Date: 2025-01-09 DOI: 10.1016/j.mito.2025.102004

Luz Marina Sánchez-Mendoza , José A. González-Reyes , Sandra Rodríguez-López , Miguel Calvo-Rubio , Pilar Calero-Rodríguez , Rafael de Cabo , M. Isabel Burón , José M. Villalba

{"title":"Sex-dependent adaptations in heart mitochondria from transgenic mice overexpressing cytochrome b5 reductase-3","authors":"Luz Marina Sánchez-Mendoza , José A. González-Reyes , Sandra Rodríguez-López , Miguel Calvo-Rubio , Pilar Calero-Rodríguez , Rafael de Cabo , M. Isabel Burón , José M. Villalba","doi":"10.1016/j.mito.2025.102004","DOIUrl":"10.1016/j.mito.2025.102004","url":null,"abstract":"<div><h3>Summary</h3><div>Cytochrome <em>b</em><sub>5</sub> reductase 3 (CYB5R3) overexpression upregulates mitochondrial biogenesis, function, and abundance in skeletal muscle and kidneys, and mimics some of the salutary effects of calorie restriction, with the most striking effects being observed in females. We aimed to investigate the mitochondrial adaptations prompted by CYB5R3 overexpression in the heart, an organ surprisingly overlooked in studies focused on this long-lived transgenic model despite the critical role played by CYB5R3 in supporting cardiomyocytes mitochondrial respiration. Given that CYB5R3 effects have been found to be sex-dependent, we focused our research on both males and females. CYB5R3 was efficiently overexpressed in cardiac tissue from transgenic mice, without any difference between sexes. The abundance of electron transport chain complexes markers and cytochrome <em>c</em> was higher in males than in females. CYB5R3 overexpression downregulated the levels of complexes markers in males but not females, without decreasing oxygen consumption capacity. CYB5R3 increased the size and abundance of cardiomyocytes mitochondria, and reduced thickness and preserved the length of mitochondria-endoplasmic reticulum contact sites in heart from males but not females. Metabolic changes were also highlighted in transgenic mice, with an upregulation of fatty acid oxidation markers, particularly in males. Our results support that CYB5R3 overexpression upregulates markers consistent with enhanced mitochondrial function in the heart, producing most of these actions in males, with illustrates the complexity of the CYB5R3-overexpressing transgenic model.</div></div>","PeriodicalId":18606,"journal":{"name":"Mitochondrion","volume":"81 ","pages":"Article 102004"},"PeriodicalIF":3.9,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142965830","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Reactive oxygen species favors Varicellovirus bovinealpha 5 (BoAHV-5) replication in neural cells 活性氧有利于牛痘病毒5 （BoAHV-5）在神经细胞中的复制。

IF 3.9 3区生物学

Mitochondrion Pub Date : 2025-03-01 Epub Date: 2025-01-06 DOI: 10.1016/j.mito.2025.102005

Juan José Rosales , María Belén Brunner , Marcelo Rodríguez , Maia Marin , Eduardo Néstor Maldonado , Sandra Pérez

{"title":"Reactive oxygen species favors Varicellovirus bovinealpha 5 (BoAHV-5) replication in neural cells","authors":"Juan José Rosales , María Belén Brunner , Marcelo Rodríguez , Maia Marin , Eduardo Néstor Maldonado , Sandra Pérez","doi":"10.1016/j.mito.2025.102005","DOIUrl":"10.1016/j.mito.2025.102005","url":null,"abstract":"<div><div><em>Varicellovirus bovinealpha</em> (BoAHV) 1 and 5 are closely related neurotropic alphaherpesviruses with distinct neuropathogenic potential. BoAHV-5 causes meningoencephalitis in calves whereas encephalitis by BoAHV-1 infection is sporadic. the mechanisms underlying the differences in tropism and clinical outcomes of the infections are not yet completely understood. Here, we used neuroblastoma SH-SY5Y cells as non-differentiated in comparison with the SH-SY5Y neuronal-like cells obtained after exposing SH-SY5Y undifferentiated cells to <em>trans</em>-retinoic acid. We aimed to establish whether there was a relationship between the production of reactive oxygen species (ROS) and the kinetics of virus replication. We demonstrated that ROS production after BoAHV infection was higher in differentiated cells. Generation of ROS was also dependent on the infecting BoAHV strain. Higher ROS levels were produced during BoAHV-5 infection concomitantly with enhanced viral replication. We propose that increased ROS production mechanistically contributes to the tissue damage and neuroinflammation induced by BoAHV-5 infection. Future studies will determine specific targets of ROS that mediate the effects on viral replication.</div></div>","PeriodicalId":18606,"journal":{"name":"Mitochondrion","volume":"81 ","pages":"Article 102005"},"PeriodicalIF":3.9,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142951500","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

The role of mitochondrial DNA variants and dysfunction in the pathogenesis and progression of multiple sclerosis 线粒体DNA变异和功能障碍在多发性硬化症发病和进展中的作用。

IF 3.9 3区生物学

Mitochondrion Pub Date : 2025-03-01 Epub Date: 2024-12-26 DOI: 10.1016/j.mito.2024.102002

Ramyar Rahimi Darehbagh , Shaghayegh Khanmohammadi , Nima Rezaei

{"title":"The role of mitochondrial DNA variants and dysfunction in the pathogenesis and progression of multiple sclerosis","authors":"Ramyar Rahimi Darehbagh , Shaghayegh Khanmohammadi , Nima Rezaei","doi":"10.1016/j.mito.2024.102002","DOIUrl":"10.1016/j.mito.2024.102002","url":null,"abstract":"<div><div>Multiple sclerosis (MS) is a chronic autoimmune disease that affects the central nervous system (CNS). The etiology of MS remains elusive, with a complex interplay of genetic and environmental factors contributing to its pathogenesis. Recent studies showed mitochondrial DNA (mtDNA) as a potential player in the development and progression of MS. These studies encompassed mtDNA variants, copy number variations, and haplogroups. This narrative review aims to synthesize the current understanding of the role of mtDNA’s in MS. The findings of this review suggest that mtDNA may indeed play a role in the development and progression of MS. Several studies have reported an association between mtDNA variants and increased susceptibility to MS, while others have found a link between mtDNA copy number variations and disease severity. Furthermore, specific mtDNA haplogroups have been demonstrated to confer protection against MS. MtDNA alterations may make neurons and oligodendrocytes more susceptible to inflammatory and oxidative stress, causing demyelination and axonal degeneration in MS patients. In conclusion, this review underscores the potential significance of mtDNA in the pathogenesis of MS and highlights the need for further research to fully elucidate its role. A deeper understanding of mtDNA’s involvement in MS may pave the way for the development of novel therapeutic strategies to combat this debilitating disease.</div></div>","PeriodicalId":18606,"journal":{"name":"Mitochondrion","volume":"81 ","pages":"Article 102002"},"PeriodicalIF":3.9,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142896136","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Scientific investigation of non-coding RNAs in mitochondrial epigenetic and aging disorders: Current nanoengineered approaches for their therapeutic improvement 线粒体表观遗传和衰老疾病中的非编码 RNA 科学调查：目前用于改善治疗的纳米工程方法。

IF 3.9 3区生物学

Mitochondrion Pub Date : 2025-01-01 Epub Date: 2024-11-05 DOI: 10.1016/j.mito.2024.101979

Vaibhav Patange , Kailash Ahirwar , Tripti Tripathi , Pratima Tripathi , Rahul Shukla

{"title":"Scientific investigation of non-coding RNAs in mitochondrial epigenetic and aging disorders: Current nanoengineered approaches for their therapeutic improvement","authors":"Vaibhav Patange , Kailash Ahirwar , Tripti Tripathi , Pratima Tripathi , Rahul Shukla","doi":"10.1016/j.mito.2024.101979","DOIUrl":"10.1016/j.mito.2024.101979","url":null,"abstract":"<div><div>Genetic control is vital for the growth of cells and tissues, and it also helps living things, from single-celled organisms to complex creatures, maintain a stable internal environment. Within cells, structures called mitochondria act like tiny power plants, producing energy and keeping the cell balanced. The two primary categories of RNA are messenger RNA (mRNA) and non-coding RNA (ncRNA). mRNA carries the instructions for building proteins, while ncRNA does various jobs at the RNA level. There are different kinds of ncRNA, each with a specific role. Some help put RNA molecules together correctly, while others modify other RNAs or cut them into smaller pieces. Still others control how much protein is made from a gene. Scientists have recently discovered many more ncRNAs than previously known, and their functions are still being explored. This article analyzes the RNA molecules present within mitochondria, which have a crucial purpose in the operation of mitochondria. We’ll also discuss how genes can be turned on and off without changing their DNA code, and how this process might be linked to mitochondrial RNA. Finally, we’ll explore how scientists are using engineered particles to silence genes and develop new treatments based on manipulating ncRNA.</div></div>","PeriodicalId":18606,"journal":{"name":"Mitochondrion","volume":"80 ","pages":"Article 101979"},"PeriodicalIF":3.9,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142591231","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Impact of missense mutations on the structure–function relationship of human succinyl-CoA synthetase using in silico analysis 利用硅学分析方法研究错义突变对人类琥珀酰-CoA 合成酶结构-功能关系的影响。

IF 3.9 3区生物学

Mitochondrion Pub Date : 2025-01-01 Epub Date: 2024-11-03 DOI: 10.1016/j.mito.2024.101978

Selma Elabed , Olfa Alila Fersi , Abdelaziz Tlili , Ahmed Fendri , Faiza Fakhfakh

{"title":"Impact of missense mutations on the structure–function relationship of human succinyl-CoA synthetase using in silico analysis","authors":"Selma Elabed , Olfa Alila Fersi , Abdelaziz Tlili , Ahmed Fendri , Faiza Fakhfakh","doi":"10.1016/j.mito.2024.101978","DOIUrl":"10.1016/j.mito.2024.101978","url":null,"abstract":"<div><div>The encephalomyopathic mtDNA depletion syndrome with methylmalonic aciduria is associated with succinyl-CoA synthetase (SCS) deficiency caused by pathogenic variants in genes encoding its two subunits. SCS is a mitochondrial enzyme involved in several metabolic pathways and acts as a heterodimer composed of α and β subunits encoded by <em>SUCLG1</em> and <em>SUCLA2</em> genes, respectively. The purpose of this study was to analyze the effects of the most pathogenic non-synonymous single nucleotide polymorphisms (nsSNPs) by applying, using different prediction tools, a filtering strategy, on the 343 and 365 nsSNPs found in <em>SUCLG1</em> and <em>SUCLA2</em> genes, respectively, retrieved from the databases, then to evaluate their structural and functional effects using homology modeling and molecular docking. Results showed that most deleterious mutations selected for structural analysis were located in loop regions critical for protein stability and function, especially, variants altering glycine and proline residues in these regions supporting their importance. We also showed that variants leading to hydrophobic and hydrophilic residues can destabilize the folding and binding of the protein. Molecular docking has also been used to identify the most important regions of ligand binding site (CoA binding site, ADP-Mg<sup>2+</sup> binding site and phosphate ion binding site) and between the two subunits themselves, which mainly involving the ligase CoA domain. Our structural analysis, performed on selected nsSNP, are in accordance with experimental studies reported in the literature and predicted that they would responsible to either nonfunctional protein, subunit instability resulting in reduced amounts of misassembled protein, or in a protein unable to phosphorylate ADP.</div></div>","PeriodicalId":18606,"journal":{"name":"Mitochondrion","volume":"80 ","pages":"Article 101978"},"PeriodicalIF":3.9,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142580946","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

The multifaceted modulation of mitochondrial metabolism in tumorigenesis 肿瘤发生过程中线粒体代谢的多方面调节。

IF 3.9 3区生物学

Mitochondrion Pub Date : 2025-01-01 Epub Date: 2024-11-04 DOI: 10.1016/j.mito.2024.101977

Keerthiga Rajendiran , Yafang Xie , De-Sheng Pei , Ailing Fu

{"title":"The multifaceted modulation of mitochondrial metabolism in tumorigenesis","authors":"Keerthiga Rajendiran , Yafang Xie , De-Sheng Pei , Ailing Fu","doi":"10.1016/j.mito.2024.101977","DOIUrl":"10.1016/j.mito.2024.101977","url":null,"abstract":"<div><div>Changes in mitochondrial metabolism produce a malignant transformation from normal cells to tumor cells. Mitochondrial metabolism, comprising bioenergetic metabolism, biosynthetic process, biomolecular decomposition, and metabolic signal conversion, obviously forms a unique sign in the process of tumorigenesis. Several oncometabolites produced by mitochondrial metabolism maintain tumor phenotype, which are recognized as tumor indicators. The mitochondrial metabolism synchronizes the metabolic and genetic outcome to the potent tumor microenvironmental signals, thereby further promoting tumor initiation. Moreover, the bioenergetic and biosynthetic metabolism within tumor mitochondria orchestrates dynamic contributions toward cancer progression and invasion. In this review, we describe the contribution of mitochondrial metabolism in tumorigenesis through shaping several hallmarks such as microenvironment modulation, plasticity, mitochondrial calcium, mitochondrial dynamics, and epithelial-mesenchymal transition. The review will provide a new insight into the abnormal mitochondrial metabolism in tumorigenesis, which will be conducive to tumor prevention and therapy through targeting tumor mitochondria.</div></div>","PeriodicalId":18606,"journal":{"name":"Mitochondrion","volume":"80 ","pages":"Article 101977"},"PeriodicalIF":3.9,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142591232","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Cumulative effects of mutation accumulation on mitochondrial function and fitness 突变积累对线粒体功能和健康的累积效应。

IF 3.9 3区生物学

Mitochondrion Pub Date : 2025-01-01 Epub Date: 2024-10-31 DOI: 10.1016/j.mito.2024.101976

Frédérique Paquin , Melania E. Cristescu , Pierre U. Blier , Hélène Lemieux , France Dufresne

{"title":"Cumulative effects of mutation accumulation on mitochondrial function and fitness","authors":"Frédérique Paquin , Melania E. Cristescu , Pierre U. Blier , Hélène Lemieux , France Dufresne","doi":"10.1016/j.mito.2024.101976","DOIUrl":"10.1016/j.mito.2024.101976","url":null,"abstract":"<div><div>The impact of mutations on the mitochondria deserves specific interest due to the crucial role played by these organelles on numerous cellular functions. This study examines the effects of repeated bottlenecks on mitochondrial function and fitness. <em>Daphnia pulex</em> mutation accumulation lines (MA) lines were maintained for over 120 generations under copper and no copper conditions. Following the MA propagation, <em>Daphnia</em> from MA lines were raised under optimal and high temperatures for two generations before assessing mitochondrial and phenotypic traits. Spontaneous mutation accumulation under copper led to a later age at maturity and lowered fecundity in the MA lines. Mitochondrial respiration was found to be 10% lower in all mutation accumulation (MA) lines as compared to the non-MA control. MtDNA copy number was elevated in MA lines compared to the control under optimal temperature suggesting a compensatory mechanism. Three MA lines propagated under low copper had very low mtDNA copy number and fitness, suggesting mutations might have affected genes involved in mtDNA replication or mitochondrial biogenesis. Overall, our study suggests that mutation accumulation had an impact on life history traits, mtDNA copy number, and mitochondrial respiration. Some phenotypic effects were magnified under high temperatures. MtDNA copy number appears to be an important mitigation factor to allow mitochondria to cope with mutation accumulation up to a certain level beyond which it can no longer compensate.</div></div>","PeriodicalId":18606,"journal":{"name":"Mitochondrion","volume":"80 ","pages":"Article 101976"},"PeriodicalIF":3.9,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142563611","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Mitochondrial mechanisms in Treg cell regulation: Implications for immunotherapy and disease treatment 调节 Treg 细胞的线粒体机制：对免疫疗法和疾病治疗的影响。

IF 3.9 3区生物学

Mitochondrion Pub Date : 2025-01-01 Epub Date: 2024-11-02 DOI: 10.1016/j.mito.2024.101975

Xiaozhen Zhao, Junmei Zhang, Caifeng Li, Weiying Kuang, Jianghong Deng, Xiaohua Tan, Chao Li, Shipeng Li

{"title":"Mitochondrial mechanisms in Treg cell regulation: Implications for immunotherapy and disease treatment","authors":"Xiaozhen Zhao, Junmei Zhang, Caifeng Li, Weiying Kuang, Jianghong Deng, Xiaohua Tan, Chao Li, Shipeng Li","doi":"10.1016/j.mito.2024.101975","DOIUrl":"10.1016/j.mito.2024.101975","url":null,"abstract":"<div><div>Regulatory T cells (Tregs) play a critical role in maintaining immune homeostasis and preventing autoimmune diseases. Recent advances in immunometabolism have revealed the pivotal role of mitochondrial dynamics and metabolism in shaping Treg functionality. Tregs depend on oxidative phosphorylation (OXPHOS) and fatty acid oxidation (FAO) to support their suppressive functions and long-term survival. Mitochondrial processes such as fusion and fission significantly influence Treg activity, with mitochondrial fusion enhancing bioenergetic efficiency and reducing reactive oxygen species (ROS) production, thereby promoting Treg stability. In contrast, excessive mitochondrial fission disrupts ATP synthesis and elevates ROS levels, impairing Treg suppressive capacity. Furthermore, mitochondrial ROS act as critical signaling molecules in Treg regulation, where controlled levels stabilize FoxP3 expression, but excessive ROS leads to mitochondrial dysfunction and immune dysregulation. Mitophagy, as part of mitochondrial quality control, also plays an essential role in preserving Treg function. Understanding the intricate interplay between mitochondrial dynamics and Treg metabolism provides valuable insights for developing novel therapeutic strategies to treat autoimmune disorders and enhance immunotherapy in cancer.</div></div>","PeriodicalId":18606,"journal":{"name":"Mitochondrion","volume":"80 ","pages":"Article 101975"},"PeriodicalIF":3.9,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142569081","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0