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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
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
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