Current Opinion in Physiology最新文献

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Coordination of mitochondrial and nuclear gene-expression regulation in health, evolution, and disease 线粒体和核基因表达调控在健康、进化和疾病中的协调作用
IF 2.5
Current Opinion in Physiology Pub Date : 2022-06-01 DOI: 10.1016/j.cophys.2022.100554
Omer Papier , Gavriel Minor , Hadar Medini, Dan Mishmar
{"title":"Coordination of mitochondrial and nuclear gene-expression regulation in health, evolution, and disease","authors":"Omer Papier ,&nbsp;Gavriel Minor ,&nbsp;Hadar Medini,&nbsp;Dan Mishmar","doi":"10.1016/j.cophys.2022.100554","DOIUrl":"10.1016/j.cophys.2022.100554","url":null,"abstract":"<div><p><span><span>Mitochondrial dysfunction has been reported in monogenic phenotypes, but also as part of common complex disorders. Explanations for the underlying mechanism of both disease types mostly focused on mutations in the open-reading frames of proteins encoded by either the mitochondrial or nuclear genomes, as well as in tRNA or ribosomal RNA genes in the mitochondrial DNA (mtDNA). Although disease-causing mutations have been identified in regulatory proteins of </span>mtDNA replication and maintenance, coordination between the regulation of mitochondrial and nuclear gene expression was only rarely considered as an explanation for mitochondrial dysfunction in diseases. Here, we review evidence suggesting that compromised coordination of mitonuclear regulation of gene expression constitutes an attractive mechanism to explain the involvement of mitochondrial dysfunction in a variety of disorders and in evolutionary processes. We discuss candidate mechanisms for coordination of mitonuclear gene expression and future avenues for their identification, with emphasis on </span>functional genomics techniques.</p></div>","PeriodicalId":52156,"journal":{"name":"Current Opinion in Physiology","volume":"27 ","pages":"Article 100554"},"PeriodicalIF":2.5,"publicationDate":"2022-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"73930422","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 1
Mitochondrial dynamics: roles in exercise physiology and muscle mass regulation 线粒体动力学:在运动生理学和肌肉质量调节中的作用
IF 2.5
Current Opinion in Physiology Pub Date : 2022-06-01 DOI: 10.1016/j.cophys.2022.100550
Andre Djalalvandi , Luca Scorrano
{"title":"Mitochondrial dynamics: roles in exercise physiology and muscle mass regulation","authors":"Andre Djalalvandi ,&nbsp;Luca Scorrano","doi":"10.1016/j.cophys.2022.100550","DOIUrl":"10.1016/j.cophys.2022.100550","url":null,"abstract":"<div><p><span><span>How mitochondria alter their morphology to meet cellular demands epitomizes the ‘form follows function’ architectural principle. These remodeling events are collectively termed ‘mitochondrial dynamics’. The influence of mitochondrial dynamics and of the mitochondria-shaping proteins that control it on skeletal muscle physiology has become clearer. </span>Endurance exercise prompts mitochondrial morphological changes that augment the respiratory capacity of the worked muscles. Mechanistically, exercise training increases </span>mitochondrial fusion<span> protein levels in skeletal muscle to promote the development of a hyperfused mitochondrial network that possesses denser cristae. Conversely, disruptions to the mitochondrial network through imbalances in mitochondrial dynamics lead to muscle atrophy. Insight into the connection between mitochondrial morphology and muscle-mass maintenance will help to pinpoint therapeutic targets that can be exploited to counteract sarcopenia and muscle atrophy in pathological conditions.</span></p></div>","PeriodicalId":52156,"journal":{"name":"Current Opinion in Physiology","volume":"27 ","pages":"Article 100550"},"PeriodicalIF":2.5,"publicationDate":"2022-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"75044828","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 2
Remodeling of cardiac metabolism in heart failure with preserved ejection fraction 保留射血分数的心力衰竭患者心脏代谢的重构
IF 2.5
Current Opinion in Physiology Pub Date : 2022-06-01 DOI: 10.1016/j.cophys.2022.100559
Akira Yoshii, Rong Tian
{"title":"Remodeling of cardiac metabolism in heart failure with preserved ejection fraction","authors":"Akira Yoshii,&nbsp;Rong Tian","doi":"10.1016/j.cophys.2022.100559","DOIUrl":"10.1016/j.cophys.2022.100559","url":null,"abstract":"<div><p>The remodeling of cardiac metabolism<span>, such as changes in substrate utilization and mitochondrial dysfunction, has long been suggested to impair myocardial energetics that leads to energy starvation of the failing hearts. However, most of the studies to date focused on heart failure with reduced ejection fraction<span> and the role of metabolism in the development of heart failure with preserved ejection fraction (HFpEF) is thus not well defined. Studies of cardiac metabolism in HFpEF are emerging with the recent progress in animal models. This review seeks to provide an overview of metabolic profile in HFpEF hearts from available reports and to highlight future research directions.</span></span></p></div>","PeriodicalId":52156,"journal":{"name":"Current Opinion in Physiology","volume":"27 ","pages":"Article 100559"},"PeriodicalIF":2.5,"publicationDate":"2022-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"82327365","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 1
Mitochondrial lysine acylation and cardiometabolic stress: truth or consequence? 线粒体赖氨酸酰化与心脏代谢应激:真相还是后果?
IF 2.5
Current Opinion in Physiology Pub Date : 2022-06-01 DOI: 10.1016/j.cophys.2022.100551
Deborah M Muoio , Ashley S Williams , Paul A Grimsrud
{"title":"Mitochondrial lysine acylation and cardiometabolic stress: truth or consequence?","authors":"Deborah M Muoio ,&nbsp;Ashley S Williams ,&nbsp;Paul A Grimsrud","doi":"10.1016/j.cophys.2022.100551","DOIUrl":"10.1016/j.cophys.2022.100551","url":null,"abstract":"<div><p><span>Disruptions in oxidative metabolism<span><span> are often accompanied by tissue accumulation of catabolic carbon intermediates, including acyl </span>CoA<span> molecules that can react with the epsilon amino group of lysine residues on cellular proteins. In general, acyl-lysine post-translational modifications (PTMs) on mitochondrial proteins<span> correlate negatively with energy homeostasis and are offset by the mitochondrial sirtuins, a prominent family of NAD</span></span></span></span><sup>+</sup><span>-dependent deacylases linked favorably to longevity and metabolic resilience. Whereas studies over the past decade elicited widespread conjecture as to the far-reaching regulatory roles of these PTMs, more recent work has stirred controversy in this field of study. This review draws attention to discrepancies in the science, challenges current dogma, and encourages new perspectives on the physiological relevance of mitochondrial lysine acylation.</span></p></div>","PeriodicalId":52156,"journal":{"name":"Current Opinion in Physiology","volume":"27 ","pages":"Article 100551"},"PeriodicalIF":2.5,"publicationDate":"2022-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"80348402","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 1
The integrated stress response as a key pathway downstream of mitochondrial dysfunction 综合应激反应是线粒体功能障碍下游的关键途径
IF 2.5
Current Opinion in Physiology Pub Date : 2022-06-01 DOI: 10.1016/j.cophys.2022.100555
Maria Bilen , Sara Benhammouda , Ruth S Slack , Marc Germain
{"title":"The integrated stress response as a key pathway downstream of mitochondrial dysfunction","authors":"Maria Bilen ,&nbsp;Sara Benhammouda ,&nbsp;Ruth S Slack ,&nbsp;Marc Germain","doi":"10.1016/j.cophys.2022.100555","DOIUrl":"10.1016/j.cophys.2022.100555","url":null,"abstract":"<div><p><span>Mitochondrial function is fundamental to maintaining metabolic homeostasis. Alterations in </span>mitochondrial biogenesis<span><span>, energy production, and dynamics are behind many metabolic diseases affecting particularly the muscular and nervous systems. Therefore, synchronized coordination between organelles is required to sustain homeostasis. The integrated stress response (ISR) is a heavily investigated pathway that allows for communication between organelles, including the mitochondria and the nucleus among others. The ISR slows down protein synthesis in the cytoplasm and modifies the </span>transcriptome<span> in the nucleus following mitochondrial stress. With the help of the ATF4<span> transcription factor, it promotes metabolic rewiring, amino acid, and antioxidant synthesis to counteract cellular stress. Under chronic stress, the ISR leads to apoptotic cell death. However, the mechanisms as to how the ISR can coordinate cell death and survival depending on the type of insult remain unclear. In this review, we will discuss the mechanisms of activation of the ISR under different mitochondrial dysfunctions. We propose a few mechanisms and factors that contribute to the cell-specific response. Finally, we discuss the role of the ISR in neurodegenerative diseases given the important implications of the mitochondria in maintaining healthy neurological function.</span></span></span></p></div>","PeriodicalId":52156,"journal":{"name":"Current Opinion in Physiology","volume":"27 ","pages":"Article 100555"},"PeriodicalIF":2.5,"publicationDate":"2022-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"82165525","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 8
Therapeutic mitochondrial transplantation 治疗性线粒体移植
IF 2.5
Current Opinion in Physiology Pub Date : 2022-06-01 DOI: 10.1016/j.cophys.2022.100558
James D McCully , Pedro J del Nido , Sitaram M Emani
{"title":"Therapeutic mitochondrial transplantation","authors":"James D McCully ,&nbsp;Pedro J del Nido ,&nbsp;Sitaram M Emani","doi":"10.1016/j.cophys.2022.100558","DOIUrl":"10.1016/j.cophys.2022.100558","url":null,"abstract":"<div><p><span>Ischemia-reperfusion injury can occur in a variety of organs resulting in deleterious effects that significantly compromise cellular function and viability. Mitochondria have been shown to play a major role in the consequential endpoints resulting from ischemia and reperfusion injury. In a series of studies, we have developed a novel therapeutic intervention to ameliorate the effects ischemia-reperfusion injury on mitochondria through organelle transplantation, specifically mitochondrial transplantation. In this mini-review, prepared for a broad audience, the current literature and scope of mitochondrial transplantation in experimental </span><em>in vitro</em> and animal studies and from a recent clinical study in human pediatric patients are presented.</p></div>","PeriodicalId":52156,"journal":{"name":"Current Opinion in Physiology","volume":"27 ","pages":"Article 100558"},"PeriodicalIF":2.5,"publicationDate":"2022-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"90045714","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 5
Heat and mitochondrial bioenergetics 热与线粒体生物能量学
IF 2.5
Current Opinion in Physiology Pub Date : 2022-06-01 DOI: 10.1016/j.cophys.2022.100553
Alex T Von Schulze , Paige C Geiger
{"title":"Heat and mitochondrial bioenergetics","authors":"Alex T Von Schulze ,&nbsp;Paige C Geiger","doi":"10.1016/j.cophys.2022.100553","DOIUrl":"10.1016/j.cophys.2022.100553","url":null,"abstract":"<div><p>Recurrent heat treatment (HT) is known to improve mitochondrial respiratory function<span><span> and reduce mitochondrial reactive oxygen species (mROS) production over time. Counterintuitively, HT results in acute mitochondrial stress characterized by impaired mitochondrial respiratory function and increased mROS production. The combination of reduced adenosine triphosphate (ATP) synthesis and elevated mROS production leads to the activation of the adenosine monophosphate (AMP)-activated protein kinase, nuclear factor erythroid-2-related factor 2, proliferator-activated receptor gamma coactivator 1-alpha, and nuclear respiratory factor-1 signaling cascades, as well as the heat-shock response via activation of heat-shock factor 1. The coordinated transcriptional control of these proteins leads to the chronological induction of mitochondrial quality-control mechanisms, such as mitophagy and chaperone-mediated autophagy, and mitochondrial biogenesis/remodeling. Taken together, the </span>acute stress imposed by HT leads to positive adaptations in mitochondrial health and function over time — making HT an attractive, nonpharmacologic treatment option for conditions characterized by mitochondrial dysfunction.</span></p></div>","PeriodicalId":52156,"journal":{"name":"Current Opinion in Physiology","volume":"27 ","pages":"Article 100553"},"PeriodicalIF":2.5,"publicationDate":"2022-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"73678965","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 2
Editorial overview: Mitochondrial physiology 编辑概述:线粒体生理学
IF 2.5
Current Opinion in Physiology Pub Date : 2022-06-01 DOI: 10.1016/j.cophys.2022.100538
Iain Scott, Kelsey Fisher-Wellman
{"title":"Editorial overview: Mitochondrial physiology","authors":"Iain Scott,&nbsp;Kelsey Fisher-Wellman","doi":"10.1016/j.cophys.2022.100538","DOIUrl":"10.1016/j.cophys.2022.100538","url":null,"abstract":"","PeriodicalId":52156,"journal":{"name":"Current Opinion in Physiology","volume":"27 ","pages":"Article 100538"},"PeriodicalIF":2.5,"publicationDate":"2022-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"74300988","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Integrating Sex and Gender in Mitochondrial Science 整合性与性别在线粒体科学
IF 2.5
Current Opinion in Physiology Pub Date : 2022-04-01 DOI: 10.1016/j.cophys.2022.100536
A. Junker, R. Juster, M. Picard
{"title":"Integrating Sex and Gender in Mitochondrial Science","authors":"A. Junker, R. Juster, M. Picard","doi":"10.1016/j.cophys.2022.100536","DOIUrl":"https://doi.org/10.1016/j.cophys.2022.100536","url":null,"abstract":"","PeriodicalId":52156,"journal":{"name":"Current Opinion in Physiology","volume":"22 1","pages":""},"PeriodicalIF":2.5,"publicationDate":"2022-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"81767836","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 1
How chromatin stiffens fibroblasts 染色质如何使成纤维细胞变硬
IF 2.5
Current Opinion in Physiology Pub Date : 2022-04-01 DOI: 10.1016/j.cophys.2022.100537
Shuaishuai Hu, Thomas M Vondriska
{"title":"How chromatin stiffens fibroblasts","authors":"Shuaishuai Hu,&nbsp;Thomas M Vondriska","doi":"10.1016/j.cophys.2022.100537","DOIUrl":"10.1016/j.cophys.2022.100537","url":null,"abstract":"<div><p>Fibroblasts are central to the acute and chronic response of tissues to stress: they are necessary for wound healing, involved in inflammatory responses and critical for long-term remodeling of tissue. These diverse roles of fibroblasts arise from the cells’ ability to respond to internal and extracellular cues regarding the physical state of the host tissue. In this article, we review recent evidence for the role of chromatin as a sensor of cellular stress and chromatin-dependent gene regulatory events that may be essential for fibroblast activation in the setting of injury. This emerging evidence highlights chromatin structure and accessibility as features necessary for our understanding of how cell-type-specific epigenomes sense and respond to stress.</p></div>","PeriodicalId":52156,"journal":{"name":"Current Opinion in Physiology","volume":"26 ","pages":"Article 100537"},"PeriodicalIF":2.5,"publicationDate":"2022-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9380867/pdf/nihms-1829481.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40621671","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 1
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