title: Autophagy: An Exposing Therapeutic Target in Atherosclerosis.
abstract: Autophagy is an evolutionarily conserved catabolic process whereby the cytoplasmic contents of a cell are sequestered within autophagosomes through a lysosome-dependent pathway. Increasing evidence shows that this process is of great importance in a wide range of diseases, including atherosclerosis (AS). Autophagy can be modulated in advanced AS plaques by cytokines, reactive lipids, lipopolysaccharides, advanced glycation end products, and microRNAs. Autophagy exerts both protective and detrimental functions in vascular disorders. However, despite an increasing interest in autophagy, it remains an underestimated and overlooked phenomenon in AS. Therefore, the precise role of autophagy and its relationship with apoptosis need to be described. This review highlights recent findings on the autophagy activities and signaling pathways in endothelial cells, macrophages, and smooth muscle cells that are accompanied by apoptosis in AS. We conclude with recent studies on autophagy modulation as a new therapeutic approach to treat AS.
authors.affiliation: *Zhongguancun Open Laboratory of the Research and Development of Natural Medicine and Health Products; †Key Laboratory of Bioactive Substances and Resources Utilization of Chinese Herbal Medicine, Ministry of Education; ‡Beijing Key Laboratory of Innovative Drug Discovery of Traditional Chinese Medicine (Natural Medicine) and Translational Medicine, Institute of Medicinal Plant Development, Peking Union Medical College and Chinese Academy of Medical Sciences, Beijing, China; and §Pharmaceutical College, Harbin University of Commerce, Harbin, China.
authors.forename: Yun
authors.initials: Y
authors.lastname: Luo
authors.forename: Shan
authors.initials: S
authors.lastname: Lu
authors.forename: Ping
authors.initials: P
authors.lastname: Zhou
authors.forename: Qi-Di
authors.initials: QD
authors.lastname: Ai
authors.forename: Gui-Bo
authors.initials: GB
authors.lastname: Sun
authors.forename: Xiao-Bo
authors.initials: XB
authors.lastname: Sun
mesh_terms: D000818:Animals; D017209:Apoptosis / Q000187:drug effects; D050197:Atherosclerosis / Q000188:drug therapy* / Q000378:metabolism / Q000473:pathology; D001343:Autophagy / Q000187:drug effects*; D002317:Cardiovascular Agents / Q000627:therapeutic use*; D055808:Drug Discovery; D042783:Endothelial Cells / Q000187:drug effects* / Q000378:metabolism / Q000473:pathology; D006801:Humans; D008264:Macrophages / Q000187:drug effects* / Q000378:metabolism / Q000473:pathology; D058990:Molecular Targeted Therapy; D032389:Myocytes, Smooth Muscle / Q000187:drug effects* / Q000378:metabolism / Q000473:pathology; D015398:Signal Transduction / Q000187:drug effects
chemical_list: D002317:Cardiovascular Agents