Role of autophagy in advanced atherosclerosis
Author(s) -
Yu-Ning Zhu,
Wenjing Fan,
Chi Zhang,
Fang Guo,
Wei Li,
Yufei Wang,
Zhisheng Jiang,
Shunlin Qu
Publication year - 2017
Publication title -
molecular medicine reports
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.727
H-Index - 56
eISSN - 1791-3004
pISSN - 1791-2997
DOI - 10.3892/mmr.2017.6403
Subject(s) - autophagy , autophagosome , microbiology and biotechnology , biology , lysosome , cell , phagosome , foam cell , cytoplasm , programmed cell death , organelle , cell cycle , homeostasis , macrophage , apoptosis , phagocytosis , biochemistry , in vitro , enzyme
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.
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