期刊
BIOLOGICAL REVIEWS
卷 97, 期 5, 页码 1844-1867出版社
WILEY
DOI: 10.1111/brv.12866
关键词
atherosclerosis; endothelial cells; vascular smooth muscle cells; macrophages; adipose-derived mesenchymal stem cells; senescence; dyslipidemia
类别
资金
- National Natural Science Foundation of China [81270956, 81470577]
- Fundamental Research Funds for the Central Universities of Central South University [2021zzts0377]
- project of Health Commission of Hunan Province, China [202203012938]
- Natural Science Foundation of Changsha City, Hunan, China [kq2202393]
Atherosclerosis is an age-related disease and a leading cause of mortality worldwide. Recent studies have shown that cellular senescence contributes to the development of atherosclerosis. Dyslipidemia plays a critical role in both cellular senescence and atherosclerosis.
Atherosclerosis, characterized by lipid-rich plaques in the arterial wall, is an age-related disorder and a leading cause of mortality worldwide. However, the specific mechanisms remain complex. Recently, emerging evidence has demonstrated that senescence of various types of cells, such as endothelial cells (ECs), vascular smooth muscle cells (VSMCs), macrophages, endothelial progenitor cells (EPCs), and adipose-derived mesenchymal stem cells (AMSCs) contributes to atherosclerosis. Cellular senescence and atherosclerosis share various causative stimuli, in which dyslipidemia has attracted much attention. Dyslipidemia, mainly referred to elevated plasma levels of atherogenic lipids or lipoproteins, or functional impairment of anti-atherogenic lipids or lipoproteins, plays a pivotal role both in cellular senescence and atherosclerosis. In this review, we summarize the current evidence for dyslipidemia-induced cellular senescence during atherosclerosis, with a focus on low-density lipoprotein (LDL) and its modifications, hydrolysate of triglyceride-rich lipoproteins (TRLs), and high-density lipoprotein (HDL), respectively. Furthermore, we describe the underlying mechanisms linking dyslipidemia-induced cellular senescence and atherosclerosis. Finally, we discuss the senescence-related therapeutic strategies for atherosclerosis, with special attention given to the anti-atherosclerotic effects of promising geroprotectors as well as anti-senescence effects of current lipid-lowering drugs.
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