Journal
SCIENCE CHINA-LIFE SCIENCES
Volume 61, Issue 9, Pages 1024-1029Publisher
SCIENCE PRESS
DOI: 10.1007/s11427-017-9285-1
Keywords
atherosclerosis; AMP-activated protein kinase; cardiovascular diseases; inflammation; autophagy
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Funding
- National Natural Science Foundation of China [91539126]
- National Science and Technology Major Project [2017ZX09101003-003-011]
- CAMS Innovation Fund for Medical Sciences [2016-I2M-1-009]
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Endothelial dysfunction is caused by many factors, such as dyslipidemia, endoplasmic reticulum (ER) stress, and inflammation. It has been demonstrated that endothelial dysfunction is the initial process of atherosclerosis. AMP-activated protein kinase (AMPK) is an important metabolic switch that plays a crucial role in lipid metabolism and inflammation. However, recent evidence indicates that AMPK could be a target for atherosclerosis by improving endothelial function. For instance, activation of AMPK inhibits the production of reactive oxygen species induced by mitochondrial dysfunction, ER stress, and NADPH oxidase. Moreover, activation of AMPK inhibits the production of pro-inflammatory factors induced by dyslipidemia and hyperglycemia and restrains production of perivascular adipose tissue-released adipokines. AMPK activation prevents endothelial dysfunction by increasing the bioavailability of nitric oxide. Therefore, we focused on the primary risk factors involved in endothelial dysfunction, and summarize the features of AMPK in the protection of endothelial function, by providing signaling pathways thought to be important in the pathological progress of risk factors.
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