Mitochondrion最新文献_第3页

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 : 2025-01-09 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":"2025-01-09","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

Yeast Dnm1G178R causes altered organelle dynamics and sheds light on the human DRP1G149R disease mechanism 酵母Dnm1G178R引起细胞器动力学改变，揭示了人类DRP1G149R疾病机制。

IF 3.9 3区生物学

Mitochondrion Pub Date : 2025-01-07 DOI: 10.1016/j.mito.2025.102006

Ankita Adhikary, Vivian Francis Joseph, Riddhi Banerjee , Shirisha Nagotu

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 : 2025-01-06 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":"2025-01-06","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

Pyridoxal-5-phosphate mitigates age-related metabolic imbalances in the rat heart through the H2S/AKT/GSK3β signaling axis 吡哆醛-5-磷酸通过H2S/AKT/GSK3β信号轴减轻大鼠心脏年龄相关的代谢失衡。

IF 3.9 3区生物学

Mitochondrion Pub Date : 2025-01-02 DOI: 10.1016/j.mito.2024.102001

Nataliia A. Strutynska , Volodymyr V. Balatskyi , Ruslan B. Strutynskyi , Yulia V. Goshovska , Lidiia A. Mys , Alina Yu. Luchkova , Maiia V. Denysova , Yuliia P. Korkach , Vladyslav R. Strutynskyi , Oksana O. Piven , Pawel Dobrzyn , Vadym F. Sagach

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 : 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":"2024-12-26","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

Autologous mitochondrial transplantation enhances the bioenergetics of auditory cells and mitigates cell loss induced by H2O2

IF 3.9 3区生物学

Mitochondrion Pub Date : 2024-12-25 DOI: 10.1016/j.mito.2024.102003

Mustafa Nazir Okur , Adam Ratajczak , Arash Kheradvar , Hamid R Djalilian

{"title":"Autologous mitochondrial transplantation enhances the bioenergetics of auditory cells and mitigates cell loss induced by H2O2","authors":"Mustafa Nazir Okur , Adam Ratajczak , Arash Kheradvar , Hamid R Djalilian","doi":"10.1016/j.mito.2024.102003","DOIUrl":"10.1016/j.mito.2024.102003","url":null,"abstract":"<div><div>Hearing loss is a widespread and disabling condition with no current cure, underscoring the urgent need for new therapeutic approaches for treatment and prevention. A recent mitochondrial therapy approach by introducing exogenous mitochondria to the cells has shown promising results in mitigating mitochondria-related disorders. Despite the essential role of mitochondria in hearing, this novel strategy has not yet been tested for the treatment of hearing loss. More importantly, whether cochlear cells take up exogenous mitochondria and its consequence on cell bioenergetics has never been tested before. Here, we showed that exogenous mitochondria from HEI-OC1 auditory cells internalize into a new set of HEI-OC1 cells through co-incubation in a dose-dependent manner without inducing toxicity. We observed that auditory cells that received exogenous mitochondria exhibited increased bioenergetics compared to the controls that received none. Furthermore, we found that mitochondrial transplantation protects cells from oxidative stress and H<sub>2</sub>O<sub>2</sub>-induced apoptosis, while partially restoring bioenergetics diminished by H<sub>2</sub>O<sub>2</sub> exposure. These findings support initial evidence for the feasibility and potential advantages of mitochondrial therapy in auditory cells. If successful in animal models and ultimately in humans, this novel therapy offers prominent potential for the treatment of sensorineural hearing loss.</div></div>","PeriodicalId":18606,"journal":{"name":"Mitochondrion","volume":"81 ","pages":"Article 102003"},"PeriodicalIF":3.9,"publicationDate":"2024-12-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143100904","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

Substitution of leucine by glutamate perturbs VopE localization to mitochondria: Lessons from yeast model system 用谷氨酸取代亮氨酸会扰乱 VopE 在线粒体的定位：酵母模型系统的启示

IF 3.9 3区生物学

Mitochondrion Pub Date : 2024-12-13 DOI: 10.1016/j.mito.2024.101999

Nandita Sharma , Kiran Heer , Saumya Raychaudhuri

引用次数: 0

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 : 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":"2024-12-09","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

Mitochondrial DNA (mtDNA) accelerates oxygen-glucose deprivation-induced injury of proximal tubule epithelia cell via inhibiting NLRC5 线粒体DNA（mtDNA）通过抑制NLRC5加速氧-葡萄糖剥夺诱导的近端肾小管上皮细胞损伤。

IF 3.9 3区生物学

Mitochondrion Pub Date : 2024-11-24 DOI: 10.1016/j.mito.2024.101989

Guojun Ge , Bocheng Zhu , Xiaofeng Zhu , Zhenfei Yu , Keqing Zhu , Mengshi Cheng

{"title":"Mitochondrial DNA (mtDNA) accelerates oxygen-glucose deprivation-induced injury of proximal tubule epithelia cell via inhibiting NLRC5","authors":"Guojun Ge , Bocheng Zhu , Xiaofeng Zhu , Zhenfei Yu , Keqing Zhu , Mengshi Cheng","doi":"10.1016/j.mito.2024.101989","DOIUrl":"10.1016/j.mito.2024.101989","url":null,"abstract":"<div><div>The high morbidity and mortality associated with acute kidney injury (AKI) are global health concerns. AKI is commonly attributed to ischemia/reperfusion injury (IRI), a condition characterized by activation of inflammatory responses and mitochondrial dysfunction. Nonetheless, mitochondrial DNA (mtDNA) has the potential to induce renal IRI. This study aimed to elucidate the mechanism and function of mtDNA in HK-2 cells that had been exposed to oxygen-glucose deprivation/reperfusion (OGD/R) and in renal IRI mice. OGD/R was discovered to induce an increase in the amount of mtDNA in HK-2 cells. Moreover, our study demonstrated that mtDNA facilitated cellular apoptosis and inflammation <em>in vivo</em> and <em>in vitro</em>. Given the potential role of inflammation in OGD/R, we investigated the effect of mtDNA on various signaling pathways associated with inflammation. Western blot analysis demonstrated that mtDNA significantly upregulated <em>NLRC5</em>/<em>TAP1</em> signaling. Furthermore, the upregulation of <em>NLRC5</em> and <em>TAP1</em> expression induced by mtDNA was reversed when <em>NLRC5</em> was inhibited. It is worth mentioning that the loss of <em>NLRC5</em> effectively nullified the beneficial effects of mtDNA on inflammation and cell apoptosis induced by OGD/R. In addition, in renal IRI mice, mtDNA treatment also aggravated inflammation and kidney damage, and increased the <em>NLRC5</em> levels in kidney tissues. These results suggested that <em>NLRC5</em> acts as an intermediary between mtDNA and the pathogenicity of renal IRI. In summary, this study provides evidence that mtDNA promotes apoptosis and inflammation in OGD/R treated HK-2 cells and renal IRI mice through upregulating <em>NLRC5</em> levels.</div></div>","PeriodicalId":18606,"journal":{"name":"Mitochondrion","volume":"81 ","pages":"Article 101989"},"PeriodicalIF":3.9,"publicationDate":"2024-11-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142716272","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

Expression of fragmented ribosomal RNA from the mitochondrial genome of Eimeria tenella 天牛埃默氏菌线粒体基因组片段核糖体 RNA 的表达。

IF 3.9 3区生物学

Mitochondrion Pub Date : 2024-11-24 DOI: 10.1016/j.mito.2024.101990

Perryn S. Kruth , Chloe MacNeil , John R. Barta

{"title":"Expression of fragmented ribosomal RNA from the mitochondrial genome of Eimeria tenella","authors":"Perryn S. Kruth , Chloe MacNeil , John R. Barta","doi":"10.1016/j.mito.2024.101990","DOIUrl":"10.1016/j.mito.2024.101990","url":null,"abstract":"<div><div>Highly fragmented ribosomal RNA-coding sequences are characteristic of mitogenomes of protozoan parasites of the phylum Apicomplexa. Identification of ribosomal RNA encoding sequences in apicomplexan mitogenomes has largely relied on sequence similarity with several apicomplexan species for which expression of these genes has been demonstrated. The present study applied Next-Gen sequencing to investigate the expression of fragmented putative mitochondrial rRNAs in <em>E. tenella</em>  <em>Plasmodium falciparum</em>  <em>E.tenella<!--> </em>mitogenome. The varied relative abundances, presence of shorter RNAs expressed from longer putative rDNA fragments, and variable polyadenylation of these sRNAs highlight additional areas for future work towards better understanding the expression of the mitogenome in this important poultry pathogen. More generally, these findings expand our wider understanding of evolution of apicomplexan mitogenomes.</div></div>","PeriodicalId":18606,"journal":{"name":"Mitochondrion","volume":"81 ","pages":"Article 101990"},"PeriodicalIF":3.9,"publicationDate":"2024-11-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142716271","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