- Author:
Shin Kyoung HUR
1
;
Seung Hee PARK
;
Goo Taeg OH
Author Information
- Publication Type:Review
- Keywords: Autophagy; Atherosclerosis; Vascular disease
- MeSH: Atherosclerosis*; Autophagy*; Cell Death; Cytoplasm; Endothelial Cells; Lysosomes; Membranes; Myocytes, Smooth Muscle; Negotiating; Plaque, Atherosclerotic; Sirolimus; Vascular Diseases
- From:Journal of Lipid and Atherosclerosis 2016;5(1):1-10
- CountryRepublic of Korea
- Language:Korean
- Abstract: Autophagy is a life-sustaining process by which cytoplasmic constituents are segregated in double-lipid bilayer membrane vesicles and undergo degradation into lysosomes. In recent studies, the basal autophagy is an indispensable process mediating proper vascular function in the body. Moreover, autophagy activated by many stress-related stimuli in the arterial wall protects endothelial cells and smooth muscle cells against cell death and the progression of vascular disease including atherosclerosis. Autophagy is protective to atherosclerosis during early stage but becomes dysfunctional in advanced atherosclerotic lesions. Following this finding, the need is emphasized which pharmacological development with compounds that activate the protective effects of autophagy in the vascular disease. Autophagy stimulated by oral or vascular delivery of rapamycin or derivatives effectively suppressed the atherosclerotic plaque growth and plaque destabilization. In this review, the recent finding is summarized on the role of autophagy in atherosclerosis and find out whether the activation or rescue of autophagy could provide a breakthrough in the treatment of atherosclerosis.