Mitochondrion最新文献_第8页

Research progress on paternal mitochondrial inheritance: An overview 父系线粒体遗传研究进展综述。

IF 3.9 3区生物学

Mitochondrion Pub Date : 2025-05-01 Epub Date: 2025-02-28 DOI: 10.1016/j.mito.2025.102019

Wen Hu , Jiting Zhang , Zhaoqi Wu , Yi Wu , Yuhui Hu , Xiaohui Hu , Jinguo Cao

{"title":"Research progress on paternal mitochondrial inheritance: An overview","authors":"Wen Hu , Jiting Zhang , Zhaoqi Wu , Yi Wu , Yuhui Hu , Xiaohui Hu , Jinguo Cao","doi":"10.1016/j.mito.2025.102019","DOIUrl":"10.1016/j.mito.2025.102019","url":null,"abstract":"<div><div>Mitochondria are self-replicating organelles with their own DNA. They play a crucial role in biological, cellular and functional processes, such as energy production, metabolism, and signal transduction. Abnormal mitochondrial function can cause various diseases such as diabetes, tumour, Parkinson’s disease, hereditary optic neuropathy, and others. Although mitochondrial functions have been extensively and widely explored, studies on mitochondrial inheritance have been limited. Mitochondrial inheritance is traditionally thought to be maternal although small amounts of paternally transmitted mitochondria have been discovered on rare occasions, and the role of paternal mitochondria transmission to offspring has been largely ignored. This review highlights the present knowledge on mitochondrial inheritance, especially the controversy and the difficulties in investigating paternal mitochondrial inheritance. More significantly, we present a comprehensive description of the physiological functions of paternal mitochondria in children and discuss the animal model to explore the mechanism of paternal mitochondrial inheritance. This review may provide a theoretical and experimental basis for improving our understanding of paternal mitochondrial inheritance, and also provide new ideas for treating mitochondrial diseases.</div></div>","PeriodicalId":18606,"journal":{"name":"Mitochondrion","volume":"82 ","pages":"Article 102019"},"PeriodicalIF":3.9,"publicationDate":"2025-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143537391","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

Mitochondria in aging and age-associated diseases 线粒体在衰老和衰老相关疾病中的作用。

IF 3.9 3区生物学

Mitochondrion Pub Date : 2025-05-01 Epub Date: 2025-02-27 DOI: 10.1016/j.mito.2025.102022

Sonu Pahal , Nirjal Mainali , Meenakshisundaram Balasubramaniam , Robert J. Shmookler Reis , Srinivas Ayyadevara

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 : 2025-03-01 Epub 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":"2025-03-01","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

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 : 2025-03-01 Epub 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

Autologous mitochondrial transplantation enhances the bioenergetics of auditory cells and mitigates cell loss induced by H2O2 自体线粒体移植可增强听觉细胞的生物能量学，减轻H2O2诱导的细胞损失

IF 3.9 3区生物学

Mitochondrion Pub Date : 2025-03-01 Epub 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":"2025-03-01","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

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 : 2025-03-01 Epub 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

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 : 2025-03-01 Epub 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":"2025-03-01","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

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 : 2025-03-01 Epub Date: 2024-12-13 DOI: 10.1016/j.mito.2024.101999

Nandita Sharma , Kiran Heer , Saumya Raychaudhuri

引用次数: 0

The unusual suspect: A novel role for intermediate filament proteins in mitochondrial morphology 不寻常的怀疑：中间丝蛋白在线粒体形态中的新作用。

IF 3.9 3区生物学

Mitochondrion Pub Date : 2025-03-01 Epub Date: 2025-02-03 DOI: 10.1016/j.mito.2025.102008

Irene M.G.M. Hemel , Carlijn Steen , Simon L.I.J. Denil , Gökhan Ertaylan , Martina Kutmon , Michiel Adriaens , Mike Gerards

引用次数: 0

Novel intronic variant in NDUFS7 gene results in mitochondrial complex I assembly defect with early basal ganglia and midbrain involvement with progressive neuroimaging findings NDUFS7基因的新内含子变异导致线粒体复合体I组装缺陷，早期基底神经节和中脑受累，伴有进行性神经影像学表现。

IF 3.9 3区生物学

Mitochondrion Pub Date : 2025-03-01 Epub Date: 2025-01-31 DOI: 10.1016/j.mito.2025.102007

Jaakko Oikarainen , Reetta Hinttala , Naemeh Nayebzadeh , Salla M. Kangas , Katariina Mankinen , Elisa Rahikkala , Hannaleena Kokkonen , Päivi Vieira , Maria Suo-Palosaari , Johanna Uusimaa

引用次数: 0