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Recent insights concerning autophagy and endothelial cell nitric oxide generation 关于自噬和内皮细胞一氧化氮生成的最新见解
IF 2.5
Current Opinion in Physiology Pub Date : 2022-12-01 DOI: 10.1016/j.cophys.2022.100614
Seul-Ki Park , Jae Min Cho , Sohom Mookherjee , Paulo W. Pires , John David Symons
{"title":"Recent insights concerning autophagy and endothelial cell nitric oxide generation","authors":"Seul-Ki Park ,&nbsp;Jae Min Cho ,&nbsp;Sohom Mookherjee ,&nbsp;Paulo W. Pires ,&nbsp;John David Symons","doi":"10.1016/j.cophys.2022.100614","DOIUrl":"10.1016/j.cophys.2022.100614","url":null,"abstract":"<div><p>Although endothelial cell (EC) dysfunction contributes to the etiology of more diseases than any other tissue in the body, EC metabolism is an understudied therapeutic target. Evidence regarding the important role of autophagy in maintaining EC homeostasis<span> is accumulating rapidly. Here, we focus on advances over the past two years regarding how EC autophagy mediates EC nitric oxide generation in the context of aging and cardiovascular complications, including coronary artery disease, aneurysm, and stroke. In addition, insight concerning the efficacy of maneuvers designed to boost EC autophagy in an effort to combat cardiovascular complications associated with repressed EC autophagy is discussed.</span></p></div>","PeriodicalId":52156,"journal":{"name":"Current Opinion in Physiology","volume":"30 ","pages":"Article 100614"},"PeriodicalIF":2.5,"publicationDate":"2022-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"78777407","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
Role of autophagy in liver diseases 自噬在肝脏疾病中的作用
IF 2.5
Current Opinion in Physiology Pub Date : 2022-12-01 DOI: 10.1016/j.cophys.2022.100594
Hideaki Morishita , Masaaki Komatsu
{"title":"Role of autophagy in liver diseases","authors":"Hideaki Morishita ,&nbsp;Masaaki Komatsu","doi":"10.1016/j.cophys.2022.100594","DOIUrl":"10.1016/j.cophys.2022.100594","url":null,"abstract":"<div><p><span>Since the initial discovery of autophagy in rat liver over 60 years ago, studies on hepatic autophagy have provided insight into the mechanisms and physiological functions of autophagy. These findings include the essential role of starvation-induced autophagy in supplying nutrients such as amino acids, glucose, and </span>free fatty acids<span> for energy production and the synthesis of macromolecules. Furthermore, it has been established that autophagy selectively degrades intracellular components such as p62/SQSTM1- and ubiquitin-containing droplets, as well as damaged organelles for intracellular quality control in hepatic cells. Dysfunction of hepatic autophagy can lead to several liver diseases, including hepatic tumors. In this review, we describe the physiological role of hepatic autophagy and its pathophysiological significance in several chronic liver disorders.</span></p></div>","PeriodicalId":52156,"journal":{"name":"Current Opinion in Physiology","volume":"30 ","pages":"Article 100594"},"PeriodicalIF":2.5,"publicationDate":"2022-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"74766775","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
Glycophagy — the physiological perspective on a newly characterized glycogen-selective autophagy 糖吞噬——一种新发现的糖原选择性自噬的生理学视角
IF 2.5
Current Opinion in Physiology Pub Date : 2022-12-01 DOI: 10.1016/j.cophys.2022.100598
Lea MD Delbridge , Parisa Koutsifeli , Sarah PT Fong , Marco Annandale , Kate L Weeks , James R Bell , Kimberley M Mellor
{"title":"Glycophagy — the physiological perspective on a newly characterized glycogen-selective autophagy","authors":"Lea MD Delbridge ,&nbsp;Parisa Koutsifeli ,&nbsp;Sarah PT Fong ,&nbsp;Marco Annandale ,&nbsp;Kate L Weeks ,&nbsp;James R Bell ,&nbsp;Kimberley M Mellor","doi":"10.1016/j.cophys.2022.100598","DOIUrl":"10.1016/j.cophys.2022.100598","url":null,"abstract":"<div><p><span>Degradation of intracellular components through autophagy is a fundamental process to maintain cellular integrity and homeostasis. Recently, a glycogen-selective autophagy pathway has been described, termed ‘glycophagy’. Glycogen is a primary storage depot and regulator of glucose availability, and glycophagy is emerging as a critical physiological process involved in energy metabolism. Glycophagy-mediated degradation of glycogen appears to operate in parallel with the well-described canonical pathway of </span>glycogenolysis<span> involving glycogen phosphorylase. Evidence suggests that starch-binding domain protein 1 (Stbd1) is a key glycogen-binding protein involved in tagging glycogen for glycophagy, and that GABA Type A Receptor Protein Like 1 is primarily involved as the Atg8 family protein recruiting the Stbd1–glycogen complex into the forming glycophagosome. The nuances of glycophagy protein machinery, regulation, and lysosomal glucose release are yet to be fully elucidated. In this mini-review, we critically analyze the current evidence base for glycophagy as a selective-autophagy process of physiological importance and highlight areas where further investigation is warranted.</span></p></div>","PeriodicalId":52156,"journal":{"name":"Current Opinion in Physiology","volume":"30 ","pages":"Article 100598"},"PeriodicalIF":2.5,"publicationDate":"2022-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"84198417","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
Mechanisms and physiological functions of ER-phagy er吞噬的机制和生理功能
IF 2.5
Current Opinion in Physiology Pub Date : 2022-12-01 DOI: 10.1016/j.cophys.2022.100613
Pablo Sanz-Martinez, Alexandra Stolz
{"title":"Mechanisms and physiological functions of ER-phagy","authors":"Pablo Sanz-Martinez,&nbsp;Alexandra Stolz","doi":"10.1016/j.cophys.2022.100613","DOIUrl":"10.1016/j.cophys.2022.100613","url":null,"abstract":"<div><p>The endoplasmic reticulum (ER) is the largest cellular organelle that undergoes constant turnover upon diverse functional demands and cellular signals. Removal of nonfunctional or superfluous subdomains is balanced by the parallel expansion and formation of ER membranes, leading to the dynamic exchange of ER components. In recent years, selective autophagy of the ER, termed ER-phagy, has emerged as a predominant process involved in ER degradation and maintenance of ER homeostasis. Identification of multiple ER-phagy receptors, many with additional ER-shaping functions, paved the way for our molecular understanding of ER turnover in different cells and organs. In this review, we describe the molecular principles underling the physiological functions of ER-phagy in maintaining ER homeostasis via receptor-mediated macroautophagy and elaborate current focus points of the field.</p></div>","PeriodicalId":52156,"journal":{"name":"Current Opinion in Physiology","volume":"30 ","pages":"Article 100613"},"PeriodicalIF":2.5,"publicationDate":"2022-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2468867322001316/pdfft?md5=cf09e9008cea36c94368138e2e807db3&pid=1-s2.0-S2468867322001316-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"87986052","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: 0
Role of autophagy in the eye: from physiology to disease 自噬在眼睛中的作用:从生理到疾病
IF 2.5
Current Opinion in Physiology Pub Date : 2022-12-01 DOI: 10.1016/j.cophys.2022.100592
Hideaki Morishita
{"title":"Role of autophagy in the eye: from physiology to disease","authors":"Hideaki Morishita","doi":"10.1016/j.cophys.2022.100592","DOIUrl":"10.1016/j.cophys.2022.100592","url":null,"abstract":"<div><p>Autophagy is a conserved catabolic process that delivers cytoplasmic materials to the lysosome for degradation. Recent studies indicate that autophagy is essential for maintaining vision by regulating intracellular homeostasis in various structures of the eye, including the lens, retina, cornea, and trabecular meshwork. Dysregulated autophagy causes ocular diseases such as cataract, glaucoma, retinitis pigmentosa, and age-related macular degeneration. Autophagy-independent degradation pathways such as LC3-associated phagocytosis in the retina and cytosolic PLAAT phospholipase-mediated organelle degradation in the lens are also physiologically important. Here, I summarize recent findings on the role of autophagy and related pathways in ocular physiology and disease.</p></div>","PeriodicalId":52156,"journal":{"name":"Current Opinion in Physiology","volume":"30 ","pages":"Article 100592"},"PeriodicalIF":2.5,"publicationDate":"2022-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2468867322001109/pdfft?md5=5188e5de08a826206a6d97dae4def8f4&pid=1-s2.0-S2468867322001109-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"84985948","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
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
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