Deficient Chaperone-Mediated Autophagy Promotes Lipid Accumulation in Macrophage

被引：29
|
作者：
Qiao, Lei [1 ,2 ]
Wang, He-feng [1 ,2 ,3 ]
Xiang, Lei [4 ]
Ma, Jing [1 ,2 ]
Zhu, Qiang [5 ]
Xu, Dan [1 ,2 ]
Zheng, Hui [1 ,2 ]
Peng, Jie-qiong [6 ]
Zhang, Sen [1 ,2 ,3 ]
Lu, Hui-xia [1 ,2 ]
Chen, Wen-qiang [1 ,2 ]
Zhang, Yun [1 ,2 ]
机构：
[1] Shandong Univ, Key Lab Cardiovasc Remodeling & Funct Res, Chinese Natl Hlth Commiss, Chinese Minist Educ,Qilu Hosp, 107 Wenhuaxi Rd, Jinan 250012, Peoples R China
[2] Shandong Univ, Chinese Acad Med Sci, State & Shandong Prov Joint Key Lab Translat Card, Dept Cardiol,Qilu Hosp, 107 Wenhuaxi Rd, Jinan 250012, Peoples R China
[3] Shandong Univ Qingdao, Qilu Hosp, 758 Hefei Rd, Qingdao 266035, Peoples R China
[4] Sishui Cty Peoples Hosp, Dept Cardiol, Sishui 273200, Shandong, Peoples R China
[5] Sishui Cty Peoples Hosp, Dept Clin Lab, Sishui 273200, Shandong, Peoples R China
[6] Univ Jinan, Shandong Acad Med Sci, Sch Med & Life Sci, Jinan, Peoples R China
来源：
JOURNAL OF CARDIOVASCULAR TRANSLATIONAL RESEARCH | 2021年 / 14卷 / 04期
基金：
中国国家自然科学基金;
关键词：
Atherosclerosis; Chaperone-mediated autophagy; Lipid metabolism; Long-chain-fatty-acid-CoA ligase 1; Lysosomal acid lipase; SCAVENGER RECEPTOR; CHOLESTEROL EFFLUX; DEGRADATION; METABOLISM; DEPOSITION; CELLS;
D O I：
10.1007/s12265-020-09986-3
中图分类号：
R5 [内科学];
学科分类号：
1002 ; 100201 ;
摘要：
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 (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 LAMP-2A (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. There were no differences in other lipid-related proteins, such as SR-A, SR-B (CD36), ABCA1, or PLIN2. 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 facilitate lipid metabolism and alleviate atherosclerosis progression. Graphical abstract
引用
收藏
页码：661 / 669
页数：9
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