Chaperone-Mediated Autophagy

Yang, Qian; Wang, Ronglin; Zhu, Lin

doi:10.1007/978-981-15-0602-4_20

Cited by 58 publications

(48 citation statements)

References 21 publications

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“…Microautophagy is a non-selective form of autophagy, through which cytoplasmic degrading materials are engulfed via invagination of the lysosomal/ vacuolar membranes (Mijaljica et al, 2011;Li and Hochstrasser, 2020). Chaperone-mediated autophagy is a selective autophagy form relying on the presentation of chaperones via certain target motif in the substrate proteins and lysosomal chaperons (Yang et al, 2019;Dash et al, 2020). Since macroautophagy is so far the most studied form of autophagy and has been reported to be involved in diseases, here in this review, we will mainly discuss the biological features of macroautophagy and its role in IBD (herein referred to as "autophagy").…”

Section: Biological Characteristics Of Autophagymentioning

confidence: 99%

The Role of Autophagy in Inflammatory Bowel Disease

et al. 2021

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Inflammatory bowel disease (IBD) is an idiopathic intestinal inflammatory disease, including ulcerative colitis (UC) and Crohn’s disease (CD). The abnormality of inflammatory and immune responses in the intestine contributes to the pathogenesis and progression of IBD. Autophagy is a vital catabolic process in cells. Recent studies report that autophagy is highly involved in various kinds of diseases, especially inflammation-related diseases, such as IBD. In this review, the biological characteristics of autophagy and its role in IBD will be described and discussed based on recent literature. In addition, several therapies for IBD through modulating the inflammasome and intestinal microbiota taking advantage of autophagy regulation will be introduced. We aim to bring new insight in the exploration of mechanisms for IBD and development of novel therapeutic strategies against IBD.

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Section: Biological Characteristics Of Autophagymentioning

confidence: 99%

The Role of Autophagy in Inflammatory Bowel Disease

et al. 2021

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“…Intracellular lipolysis is the process to hydrolyze triglycerides or cholesteryl esters to fatty acids (FAs). Apart from the classical "neutral lipolysis," which degrades lipids with the help of cytoplasmic hydrolases, another pathway called "acid lipolysis" or "lipophagy" has been identified in the past several years [17][18][19]. Lipophagy refers to degradation of lipids through autophagy-lysosome pathway [19].…”

Section: Discussionmentioning

confidence: 99%

Deficient Chaperone-Mediated Autophagy Promotes Lipid Accumulation in Macrophage

Qiao¹,

Wang

Xiang³

et al. 2020

J. of Cardiovasc. Trans. Res.

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Chaperone-mediated autophagy (CMA) serves as a critical upstream regulator of lipophagy and lipid metabolism in hepatocyte. However, the role of CMA in lipid metabolism of macrophage, the typical component of atherosclerotic plaque, remains unclear. In our study, LAMP-2A (L2A, a CMA marker) was reduced in macrophages exposed to high dose of oleate, and lipophagy was impaired in advanced atherosclerosis in ApoE (−/−) mice. Primary peritoneal macrophages isolated from macrophage-specific L2A-deficient mice exhibited pronounced intracellular lipid accumulation. Lipid regulatory enzymes, including long-chain-fattyacid-CoA ligase 1 (ACSL1) and lysosomal acid lipase (LAL), were increased and reduced in L2A-KO macrophage, respectively. Other lipid-related proteins, such as SR-A, SR-B (CD36), ABCA1, or PLIN2, were not associated with increased lipid content in L2A-KO macrophage. In conclusion, deficient CMA promotes lipid accumulation in macrophage probably by regulating enzymes involved in lipid metabolism. CMA may represent a novel therapeutic target to alleviate atherosclerosis by promoting lipid metabolism. Keywords Atherosclerosis. Chaperone-mediated autophagy. Lipid metabolism. Long-chain-fatty-acid-CoA ligase 1. Lysosomal acid lipase Abbreviations CMA Chaperone-mediated autophagy LAMP-2A Lysosome-associated membrane glycoprotein 2, isoform A OL Oleate PLIN2 Lipid-associated proteins perilipin 2 SR Scavenger receptor ABCA1 ATP-binding cassette sub family A member 1 ACSL1 Long-chain-fatty-acid-CoA ligase 1 LAL Lysosomal acid lipase Lei Qiao and He-feng Wang contributed equally to this work.

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“…As shown in Figure 1A, when the organism is under starvation, PLIN 2 and PLIN 3 can be degraded by CMA, which increases the access of lipases to neutral lipids and basal lipolysis Cuervo, 2015, 2018). In CMA, the target protein with a KFERQ motif is recognized by the heat shock cognate protein (Hsc70) complex and shuttled to the lysosomal surface, where the unfolded substrate protein is translocated into lysosomal lumen and degraded via the binding of Hsc70 and lysosome-associated membrane protein 2A (LAMP2A) (Figure 1A; Yang Q. et al, 2019). Lysosomes with CMA activity were initially extracted from starved rat livers, and reduced expression of PLIN 2 and PLIN 3 proteins in lysosomal fractions was detected, confirming that PLIN 2 and PLIN 3 are substrates of CMA.…”

Section: Degradation Of Lds Proteins By Cma Promotes Lipolysismentioning

confidence: 99%

Molecular Events Occurring in Lipophagy and Its Regulation in Flaviviridae Infection

Fan

Zou

et al. 2021

Front. Microbiol.

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Diseases caused by Flaviviridae have a wide global and economic impact due to high morbidity and mortality. Flaviviridae infection usually leads to severe, acute or chronic diseases, such as liver injury and liver cancer resulting from hepatitis C virus (HCV) infection, dengue hemorrhagic fever (DHF) or dengue shock syndrome (DSS) caused by dengue virus (DENV). Given the highly complex pathogenesis of Flaviviridae infections, they are still not fully understood at present. Accumulating evidence suggests that host autophagy is disrupted to regulate the life cycle of Flaviviridae. Organelle-specific autophagy is able to selectively target different organelles for quality control, which is essential for regulating cellular homeostasis. As an important sub process of autophagy, lipophagy regulates lipid metabolism by targeting lipid droplets (LDs) and is also closely related to the infection of a variety of pathogenic microorganisms. In this review, we briefly understand the LDs interaction relationship with Flaviviridae infection, outline the molecular events of how lipophagy occurs and the related research progress on the regulatory mechanisms of lipophagy in Flaviviridae infection. Exploring the crosstalk between viral infection and lipophagy induced molecular events may provide new avenues for antiviral therapy.

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Chaperone-Mediated Autophagy

Cited by 58 publications

References 21 publications

The Role of Autophagy in Inflammatory Bowel Disease

The Role of Autophagy in Inflammatory Bowel Disease

Deficient Chaperone-Mediated Autophagy Promotes Lipid Accumulation in Macrophage

Molecular Events Occurring in Lipophagy and Its Regulation in Flaviviridae Infection

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