title: Role of autophagy in advanced atherosclerosis (Review).
abstract: Atherosclerosis (AS) remains the leading cause for global cardiovascular disease morbidity and mortality, and a major cause of cardiopathy, myocardial infarction and peripheral vascular diseases. Macrophages serve a critical role in atherosclerotic plaque stabilization and rupture, and the selective removal of macrophages may be beneficial in improving plaque stability. Autophagy is a process of self‑feeding, during which cytoplasmic proteins or organelles are packaged into vesicles and fused with the lysosome to form an autophagosome. The newly formed autophagosome can degrade internalized proteins, and this process may be used to serve the metabolic and self‑renewal requirements of the cell. Autophagy serves an important role in maintaining cell homeostasis and promoting cell survival, and therefore an imbalance in autophagy is closely associated with multiple diseases.
authors.affiliation: Institute of Cardiovascular Disease, Key Lab for Arteriosclerology of Hunan Province, University of South China, Hengyang, Hunan 421001, P.R. China.
authors.forename: Yu-Ning
authors.initials: YN
authors.lastname: Zhu
authors.affiliation: Institute of Cardiovascular Disease, Key Lab for Arteriosclerology of Hunan Province, University of South China, Hengyang, Hunan 421001, P.R. China.
authors.forename: Wen-Jing
authors.initials: WJ
authors.lastname: Fan
authors.affiliation: Institute of Cardiovascular Disease, Key Lab for Arteriosclerology of Hunan Province, University of South China, Hengyang, Hunan 421001, P.R. China.
authors.forename: Chi
authors.initials: C
authors.lastname: Zhang
authors.affiliation: Institute of Cardiovascular Disease, Key Lab for Arteriosclerology of Hunan Province, University of South China, Hengyang, Hunan 421001, P.R. China.
authors.forename: Fang
authors.initials: F
authors.lastname: Guo
authors.affiliation: Institute of Cardiovascular Disease, Key Lab for Arteriosclerology of Hunan Province, University of South China, Hengyang, Hunan 421001, P.R. China.
authors.forename: Wei
authors.initials: W
authors.lastname: Li
authors.affiliation: Institute of Cardiovascular Disease, Key Lab for Arteriosclerology of Hunan Province, University of South China, Hengyang, Hunan 421001, P.R. China.
authors.forename: Yu-Fei
authors.initials: YF
authors.lastname: Wang
authors.affiliation: Institute of Cardiovascular Disease, Key Lab for Arteriosclerology of Hunan Province, University of South China, Hengyang, Hunan 421001, P.R. China.
authors.forename: Zhi-Sheng
authors.initials: ZS
authors.lastname: Jiang
authors.affiliation: Institute of Cardiovascular Disease, Key Lab for Arteriosclerology of Hunan Province, University of South China, Hengyang, Hunan 421001, P.R. China.
authors.forename: Shun-Lin
authors.initials: SL
authors.lastname: Qu
mesh_terms: D064007:Ataxia Telangiectasia Mutated Proteins / Q000378:metabolism; D050197:Atherosclerosis / Q000378:metabolism / Q000473:pathology*; D001343:Autophagy; D006801:Humans; D052119:Lysosomal-Associated Membrane Protein 2 / Q000378:metabolism; D008264:Macrophages / Q000276:immunology / Q000378:metabolism; D000071636:Protein Phosphatase 2C / Q000378:metabolism; D012720:Severity of Illness Index; D058570:TOR Serine-Threonine Kinases / Q000378:metabolism
chemical_list: C497811:LAMP2 protein, human; D052119:Lysosomal-Associated Membrane Protein 2; D064007:Ataxia Telangiectasia Mutated Proteins; D058570:TOR Serine-Threonine Kinases; D000071636:Protein Phosphatase 2C