Clinical Anatomy & Reproductive Medicine Application Institute, Institute of Pharmacy and Pharmacology, University of South China, Hengyang, 421001, China.
2016 Grade Excellent Doctor Class of Medical School, University of South China, Hengyang, 421001, China.
Sci China Life Sci. 2018 Oct;61(10):1212-1221. doi: 10.1007/s11427-017-9240-2. Epub 2018 Apr 12.
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.
动脉粥样硬化的特征是脂质在血管壁中积累和纤维元素的沉积，这是心血管疾病的主要原因。腺苷一磷酸激活蛋白激酶（AMPK）是能量代谢的代谢传感器，调节多种生理过程，包括脂质和葡萄糖代谢以及能量失衡的正常化。大量证据表明，AMPK 的激活显著抑制动脉粥样硬化的发展。自噬抑制细胞凋亡和炎症，促进胆固醇流出和吞噬作用。生理自噬对于维持正常心血管功能至关重要。越来越多的证据表明，自噬发生在发展中的动脉粥样硬化斑块中。新出现的证据表明，AMPK 通过下游信号通路调节自噬。由于这种与动脉粥样硬化发展的密切关系，AMPK 和自噬之间的复杂关系引起了许多研究人员的关注。本综述展示了 AMPK 和自噬在动脉粥样硬化中的作用。对这种相互关系的深入了解将为动脉粥样硬化的预防和治疗创造新的策略。
