期刊
INTERNATIONAL JOURNAL OF BIOLOGICAL SCIENCES
卷 17, 期 13, 页码 3413-3427出版社
IVYSPRING INT PUBL
DOI: 10.7150/ijbs.62506
关键词
atherosclerotic plaques; plaque instability; plaque rupture; non-coding RNAs
资金
- National Natural Science Foundation of China (China) [81870331]
- Qingdao municipal science and technology bureau project (China) [21-1-4-rkjk-12-nsh]
Cardiovascular diseases caused by arteriosclerosis are a leading global cause of death, and regulating plaque stability is crucial for reducing mortality. Recent research suggests that non-coding RNAs play a significant role in regulating the pathophysiological process of atherosclerotic plaque formation.
Cardiovascular diseases (CVDs) caused by arteriosclerosis are the leading cause of death and disability worldwide. In the late stages of atherosclerosis, the atherosclerotic plaque gradually expands in the blood vessels, resulting in vascular stenosis. When the unstable plaque ruptures and falls off, it blocks the vessel causing vascular thrombosis, leading to strokes, myocardial infarctions, and a series of other serious diseases that endanger people's lives. Therefore, regulating plaque stability is the main means used to address the high mortality associated with CVDs. The progression of the atherosclerotic plaque is a complex integration of vascular cell apoptosis, lipid metabolism disorders, inflammatory cell infiltration, vascular smooth muscle cell migration, and neovascular infiltration. More recently, emerging evidence has demonstrated that non-coding RNAs (ncRNAs) play a significant role in regulating the pathophysiological process of atherosclerotic plaque formation by affecting the biological functions of the vasculature and its associated cells. The purpose of this paper is to comprehensively review the regulatory mechanisms involved in the susceptibility of atherosclerotic plaque rupture, discuss the limitations of current approaches to treat plaque instability, and highlight the potential clinical value of ncRNAs as novel diagnostic biomarkers and potential therapeutic strategies to improve plaque stability and reduce the risk of major cardiovascular events.
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