期刊
SCIENCE CHINA-LIFE SCIENCES
卷 61, 期 10, 页码 1212-1221出版社
SCIENCE PRESS
DOI: 10.1007/s11427-017-9240-2
关键词
adenosine monophosphate-activated protein kinase; autophagy; lipid metabolism; atherosclerosis-associated cell; atherosclerosis
类别
资金
- National Natural Science Foundation of China [81670401]
- Natural Sciences Foundation of Hunan Province [2016JJ6133]
- Scientific Research Innovation Program of Post-graduate in Hunan Province [CX2017B554]
- Zhengxiang Scholar (Xiangyang Tang) Program of the University of South China
- Construct Program of the Key Discipline in Hunan Province (Basic Medicine Sciences in University of South China)
Atherosclerosis is characterized by the accumulation of lipids and deposition of fibrous elements in the vascular wall, which is the primary cause of cardiovascular diseases. Adenosine monophosphate-activated protein kinase (AMPK) is a metabolic sensor of energy metabolism that regulates multiple physiological processes, including lipid and glucose metabolism and the normalization of energy imbalances. Overwhelming evidence indicates that AMPK activation markedly attenuates atherosclerosis development. Autophagy inhibits cell apoptosis and inflammation and promotes cholesterol efflux and efferocytosis. Physiological autophagy is essential for maintaining normal cardiovascular function. Increasing evidence demonstrates that autophagy occurs in developing atherosclerotic plaques. Emerging evidence indicates that AMPK regulates autophagy via a downstream signaling pathway. The complex relationship between AMPK and autophagy has attracted the attention of many researchers because of this close relationship to atherosclerosis development. This review demonstrates the role of AMPK and autophagy in atherosclerosis. An improved understanding of this interrelationship will create novel preventive and therapeutic strategies for atherosclerosis.
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