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Transcriptional regulation of autophagy in aging 衰老过程中自噬的转录调控
IF 2.5
Current Opinion in Physiology Pub Date : 2022-10-01 DOI: 10.1016/j.cophys.2022.100591
Tatiana M Moreno , Caitlin M Lange , Caroline Kumsta
{"title":"Transcriptional regulation of autophagy in aging","authors":"Tatiana M Moreno ,&nbsp;Caitlin M Lange ,&nbsp;Caroline Kumsta","doi":"10.1016/j.cophys.2022.100591","DOIUrl":"10.1016/j.cophys.2022.100591","url":null,"abstract":"<div><p><span>Macroautophagy, hereafter autophagy, is a cellular recycling process that degrades damaged cellular components. Autophagy is important for maintaining cellular homeostasis and has been reported to decline with age. This age-related reduction in autophagy function has been associated with the development of age-related diseases. A network of </span>signaling pathways<span> that sense nutrient status and cellular stress regulate autophagy via post-translational, transcriptional, and epigenetic mechanisms, but the molecular mechanisms that lead to autophagy decline with age remain unclear. Here, we review links between autophagy and aging and focus on the hypothesis that transcriptional dysregulation of key autophagy genes contributes to the age-related decline in autophagy. We outline how transcription factors TFEB (transcription factor EB) and FOXOs ( forkhead box-O family proteins) facilitate appropriate transcriptional regulation of autophagy in healthy organisms, and summarize recent advances characterizing age-related changes in the regulation of transcription-factor function that could contribute to transcriptional dysregulation of autophagy.</span></p></div>","PeriodicalId":52156,"journal":{"name":"Current Opinion in Physiology","volume":"29 ","pages":"Article 100591"},"PeriodicalIF":2.5,"publicationDate":"2022-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"84743344","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
Drp1 and the cytoskeleton: mechanistic nexus in mitochondrial division Drp1和细胞骨架：线粒体分裂的机制联系。
IF 2.5
Current Opinion in Physiology Pub Date : 2022-10-01 DOI: 10.1016/j.cophys.2022.100574
Jason A Mears , Rajesh Ramachandran
{"title":"Drp1 and the cytoskeleton: mechanistic nexus in mitochondrial division","authors":"Jason A Mears ,&nbsp;Rajesh Ramachandran","doi":"10.1016/j.cophys.2022.100574","DOIUrl":"10.1016/j.cophys.2022.100574","url":null,"abstract":"<div><p>Dynamin-related protein 1 (Drp1), the master regulator of mitochondrial division (MD), interacts with the cytoskeletal elements, namely filamentous actin, microtubules, and septins<span> that coincidentally converge at MD sites. However, the mechanistic contributions of these critical elements to, and their cooperativity in, MD remain poorly characterized. Emergent data indicate that the cytoskeleton plays combinatorial modulator, mediator, and effector roles in MD by ‘priming’ and ‘channeling’ Drp1 for mechanoenzymatic membrane remodeling. In this brief review, we will outline our current understanding of Drp1–cytoskeleton interactions, focusing on recent progress in the field and a plausible ‘diffusion barrier’ role for the cytoskeleton in MD.</span></p></div>","PeriodicalId":52156,"journal":{"name":"Current Opinion in Physiology","volume":"29 ","pages":"Article 100574"},"PeriodicalIF":2.5,"publicationDate":"2022-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10427167","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
Autophagy in severe acute respiratory syndrome coronavirus 2 infection 严重急性呼吸综合征冠状病毒2型感染的自噬
IF 2.5
Current Opinion in Physiology Pub Date : 2022-10-01 DOI: 10.1016/j.cophys.2022.100596
Di Chen , Hong Zhang
{"title":"Autophagy in severe acute respiratory syndrome coronavirus 2 infection","authors":"Di Chen ,&nbsp;Hong Zhang","doi":"10.1016/j.cophys.2022.100596","DOIUrl":"10.1016/j.cophys.2022.100596","url":null,"abstract":"<div><p>Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) orchestrates host factors to remodel endomembrane compartments for various steps of the infection cycle. SARS-CoV-2 also intimately intersects with the catabolic autophagy pathway during infection. In response to virus infection, autophagy acts as an innate defensive system by delivering viral components/particles to lysosomes for degradation. Autophagy also elicits antiviral immune responses. SARS-CoV-2, like other positive-stranded RNA viruses, has evolved various mechanisms to escape autophagic destruction and to hijack the autophagic machinery for its own benefit. In this review, we will focus on how the interplay between SARS-CoV-2 viral proteins and autophagy promotes viral replication and transmission. We will also discuss the pathogenic effects of SARS-CoV-2-elicited autophagy dysregulation and pharmacological interventions targeting autophagy for COVID-19 treatment.</p></div>","PeriodicalId":52156,"journal":{"name":"Current Opinion in Physiology","volume":"29 ","pages":"Article 100596"},"PeriodicalIF":2.5,"publicationDate":"2022-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9514017/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10415873","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: 4
Recent insights into the role of autophagy in the heart 最近对自噬在心脏中的作用的研究
IF 2.5
Current Opinion in Physiology Pub Date : 2022-10-01 DOI: 10.1016/j.cophys.2022.100593
Wenjing Liang, Åsa B Gustafsson
{"title":"Recent insights into the role of autophagy in the heart","authors":"Wenjing Liang,&nbsp;Åsa B Gustafsson","doi":"10.1016/j.cophys.2022.100593","DOIUrl":"10.1016/j.cophys.2022.100593","url":null,"abstract":"<div><p>Terminally differentiated cardiod cells and rely on autophagy to maintain homeostasis. Autophagy is a well-known catabolic degradation process involved in eliminating lipid droplets, protein aggregates, and dysfunctional organelles. Recycling of cellular cargo also helps to maintain energy supply to meet the metabolic demand in the heart. Given this, it is not surprising that dysregulation of autophagy is implicated in the aging process and in development of cardiovascular disease. Therefore, understanding the functional role of autophagy in the heart at baseline and in various disease conditions continues to be an area of intense scientific investigation. Although consensus exists that functional autophagy is essential for cardiac homeostasis, its role in various diseases and the mechanisms underlying potential dysregulation remain unclear. Here, we review the latest insights into autophagy in cardiovascular homeostasis, aging, and disease development.</p></div>","PeriodicalId":52156,"journal":{"name":"Current Opinion in Physiology","volume":"29 ","pages":"Article 100593"},"PeriodicalIF":2.5,"publicationDate":"2022-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2468867322001110/pdfft?md5=25e4300cf817f297fa95968252ce8548&pid=1-s2.0-S2468867322001110-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"84202135","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: 2
Cardiac fibrosis in oncologic therapies 肿瘤治疗中的心脏纤维化
IF 2.5
Current Opinion in Physiology Pub Date : 2022-10-01 DOI: 10.1016/j.cophys.2022.100575
René R Sevag Packard
{"title":"Cardiac fibrosis in oncologic therapies","authors":"René R Sevag Packard","doi":"10.1016/j.cophys.2022.100575","DOIUrl":"10.1016/j.cophys.2022.100575","url":null,"abstract":"<div><p><span>Cardiotoxicity, or the development of unwarranted cardiovascular side-effects of oncologic therapies, can involve all aspects of cardiovascular disease. The development of cardiac fibrosis is a dreaded complication that leads to cardiac mechanical dysfunction, tachyarrhythmias, and an increase in </span>cardiovascular mortality<span>. This review details established and putative mechanisms, leading to fibroblast activation, myofibroblast<span> transdifferentiation, and the development of replacement or interstitial cardiac fibrosis as a consequence of cancer treatments. Clinical and imaging strategies for cardiac fibrosis assessment as well as emerging antifibrotic therapeutics will also be addressed.</span></span></p></div>","PeriodicalId":52156,"journal":{"name":"Current Opinion in Physiology","volume":"29 ","pages":"Article 100575"},"PeriodicalIF":2.5,"publicationDate":"2022-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40391537","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: 4
Mechanisms controlling selective elimination of damaged lysosomes 控制选择性消除受损溶酶体的机制
IF 2.5
Current Opinion in Physiology Pub Date : 2022-10-01 DOI: 10.1016/j.cophys.2022.100590
Melissa J Hoyer , Sharan Swarup , J Wade Harper
{"title":"Mechanisms controlling selective elimination of damaged lysosomes","authors":"Melissa J Hoyer ,&nbsp;Sharan Swarup ,&nbsp;J Wade Harper","doi":"10.1016/j.cophys.2022.100590","DOIUrl":"10.1016/j.cophys.2022.100590","url":null,"abstract":"<div><p>Lysosomes are subjected to physiological and pathophysiological insults over the course of their life cycle and are accordingly repaired or recycled. Lysophagy, the selective degradation of lysosomes via autophagy, occurs upon unrepairable lysosomal-membrane rupture; galectins bind to glycosylated macromolecules in the lysosome lumen, orchestrating a series of cellular responses to promote autophagic recycling of damaged lysosomes and transcriptional upregulation of lysosomal genes. Damaged lysosomes are ubiquitylated, resulting in the recruitment of ubiquitin-binding autophagy receptors, which promote assembly of an autophagosome around damaged lysosomes for delivery to healthy lysosomes for degradation. Here, we review the current state of our understanding of mechanisms used to mark and eliminate damaged lysosomes, and discuss the complexities of galectin function and ubiquitin-chain linkage types. Finally, we discuss the limitations of available data and challenges with the goal of understanding the mechanistic basis of key steps in lysophagic flux.</p></div>","PeriodicalId":52156,"journal":{"name":"Current Opinion in Physiology","volume":"29 ","pages":"Article 100590"},"PeriodicalIF":2.5,"publicationDate":"2022-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9878802/pdf/nihms-1865645.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10589912","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: 2
Control of unconventional secretion by the autophagy machinery 自噬机制对非常规分泌的控制
IF 2.5
Current Opinion in Physiology Pub Date : 2022-10-01 DOI: 10.1016/j.cophys.2022.100595
Tan A Nguyen , Jayanta Debnath
{"title":"Control of unconventional secretion by the autophagy machinery","authors":"Tan A Nguyen ,&nbsp;Jayanta Debnath","doi":"10.1016/j.cophys.2022.100595","DOIUrl":"10.1016/j.cophys.2022.100595","url":null,"abstract":"<div><p><span>Autophagy is a highly conserved and critical recycling and degradation pathway that involves the selective engulfment of cytoplasmic organelles and proteins into double-membrane vesicles termed autophagosomes that subsequently fuse with </span>lysosomes<span> for degradation. In addition to its established role in protein degradation, there is a growing body of evidence that in response to specific environmental cues, the autophagy machinery promotes unconventional secretion of leaderless proteins via diverse mechanisms, collectively termed ‘secretory autophagy’. In this review, we describe recent findings highlighting these noncanonical functions of the autophagy machinery in specifying vesicular cargo loading for secretion and discuss how secretory autophagy is regulated during a wide range of cellular stresses, including inflammation, starvation, and lysosomal damage.</span></p></div>","PeriodicalId":52156,"journal":{"name":"Current Opinion in Physiology","volume":"29 ","pages":"Article 100595"},"PeriodicalIF":2.5,"publicationDate":"2022-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"75162608","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
Biochemical and structural imaging of remodeled myocardium 重构心肌的生化和结构成像
IF 2.5
Current Opinion in Physiology Pub Date : 2022-08-01 DOI: 10.1016/j.cophys.2022.100570
Choukri Mekkaoui , David E Sosnovik
{"title":"Biochemical and structural imaging of remodeled myocardium","authors":"Choukri Mekkaoui ,&nbsp;David E Sosnovik","doi":"10.1016/j.cophys.2022.100570","DOIUrl":"10.1016/j.cophys.2022.100570","url":null,"abstract":"<div><p>Remodeling of the myocardium results in changes in the molecular, cellular, and microstructural properties of the heart. Traditionally, these changes have been characterized using microscopy of tissue specimens taken from the heart. However, recent advances in biomedical imaging now make it possible to characterize many of these processes noninvasively. In this review, we focus on key principles and recent advances in molecular, cellular, and microstructural imaging of the heart after ischemic injury. Techniques to image cardiomyocyte death, inflammation, fibrosis, and microstructural remodeling of the heart are highlighted.</p></div>","PeriodicalId":52156,"journal":{"name":"Current Opinion in Physiology","volume":"28 ","pages":"Article 100570"},"PeriodicalIF":2.5,"publicationDate":"2022-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"73443715","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
Mitochondrial function and dysfunction in innate immunity 线粒体功能与先天免疫功能障碍
IF 2.5
Current Opinion in Physiology Pub Date : 2022-08-01 DOI: 10.1016/j.cophys.2022.100571
Aurea Oliva , Carolina Meroño , Javier Traba
{"title":"Mitochondrial function and dysfunction in innate immunity","authors":"Aurea Oliva ,&nbsp;Carolina Meroño ,&nbsp;Javier Traba","doi":"10.1016/j.cophys.2022.100571","DOIUrl":"10.1016/j.cophys.2022.100571","url":null,"abstract":"<div><p>The mitochondria play an important role in the activation of the innate immune system. This organelle modulates the metabolic reprogramming of the immune cell into proinflammatory or anti-inflammatory subtypes, which typically utilize very different metabolic pathways to fulfill their functions. It also acts as a signaling platform to activate immune routes in both immune and nonimmune cells, as it can generate agonists for inflammatory pathways, including toll-like receptors, inflammasomes, or the cyclic GMP–AMP synthase–stimulator of interferon genes pathway, which lead to the generation of proinflammatory cytokines and antiviral molecules such as type-I interferons. These novel functions of the mitochondria are important in the fight against pathogens, but also contribute to human disease when dysregulated. This review describes recent findings in this field and highlights the role of mitochondrial nucleic acids in the regulation of innate immune signaling pathways.</p></div>","PeriodicalId":52156,"journal":{"name":"Current Opinion in Physiology","volume":"28 ","pages":"Article 100571"},"PeriodicalIF":2.5,"publicationDate":"2022-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S246886732200089X/pdfft?md5=cf921effbdcc67762a0cd063df89387a&pid=1-s2.0-S246886732200089X-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"78030959","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
State of change: epigenetic and mitochondrial regulation of cardiac fibroblast activation 改变状态:心肌成纤维细胞活化的表观遗传和线粒体调控
IF 2.5
Current Opinion in Physiology Pub Date : 2022-08-01 DOI: 10.1016/j.cophys.2022.100557
Alexandra M Garvin , Taben M Hale
{"title":"State of change: epigenetic and mitochondrial regulation of cardiac fibroblast activation","authors":"Alexandra M Garvin ,&nbsp;Taben M Hale","doi":"10.1016/j.cophys.2022.100557","DOIUrl":"10.1016/j.cophys.2022.100557","url":null,"abstract":"<div><p><span>Cardiac fibroblasts (CFs) exist in a variety of states that contribute to either conserved or uncontrolled extracellular matrix (ECM) deposition. In healthy hearts, fibroblasts favor the homeostatic or quiescent state in which they work to maintain the ECM at a baseline level of activity. Acute or chronic injury in the form of myocardial infarction, hypertension, and heart failure induce CF activation via increased pro-oxidant, proinflammatory, and profibrotic stimuli secondary to hypoxia, cardiomyocyte cell death, or hemodynamic stress. In addition to the well-described signaling molecules that induce CF activation (e.g. </span>transforming growth factor beta 1, angiotensin II, and reactive oxygen species), there are emerging concepts that describe mechanisms that regulate more nuanced transition between activation states. This review will discuss recent descriptions of heterogeneous populations of resident cardiac fibroblasts, states of fibroblast activation, and the roles for mitochondrial and chromatin accessibility in mediating transition to and persistence of the activated state.</p></div>","PeriodicalId":52156,"journal":{"name":"Current Opinion in Physiology","volume":"28 ","pages":"Article 100557"},"PeriodicalIF":2.5,"publicationDate":"2022-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"90103399","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
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