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-fatty-acid-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. Graphical abstract.
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http://dx.doi.org/10.1007/s12265-020-09986-3 | DOI Listing |
Front Biosci (Landmark Ed)
January 2025
Department of Neurology, Jinshan Hospital, Fudan University, 201508 Shanghai, China.
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Department of Biomedical Sciences, Grand Valley State University, Allendale, MI 49401, USA.
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January 2025
Department of Food Biotechnology and Microbiology, Institute of Food Sciences, Warsaw University of Life Sciences - SGGW, 02-776 Warsaw, Poland.
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Front Biosci (Landmark Ed)
January 2025
Department of Pathology, Faculty of Medicine, School of Health Sciences, University of Thessaly, 41500 Larissa, Greece.
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Front Biosci (Landmark Ed)
January 2025
The First College of Clinical Medical Science, China Three Gorges University, 443000 Yichang, Hubei, China.
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