Journal
CLINICAL CHEMISTRY AND LABORATORY MEDICINE
Volume 59, Issue 1, Pages 27-38Publisher
WALTER DE GRUYTER GMBH
DOI: 10.1515/cclm-2020-0601
Keywords
atherosclerosis; cell senescence; HVECs; HVSMCs; macrophages
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Funding
- National Natural Sciences Foundation of China [81871701, 81772244]
- Natural Science Foundation of Guangdong province-Outstanding Youth Foundation [2020B1515020013]
- NaturalScienceFoundation of Guangdong province [2017A030313535, 2018A030313533, 2017A030313532]
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Cell senescence is a key mechanism in aging and is crucial in the onset and prognosis of cardiovascular disease, fibrotic pulmonary disease, liver disease, and tumors. Additionally, it plays an indispensable role in the formation and development of atherosclerosis. Different types of senescent cells impact atherosclerosis through various pathways.
Cell senescence is a fundamental mechanism of aging and appears to play vital roles in the onset and prognosis of cardiovascular disease, fibrotic pulmonary disease, liver disease and tumor. Moreover, an increasing body of evidence shows that cell senescence plays an indispensable role in the formation and development of atherosclerosis. Multiple senescent cell types are associated with atherosclerosis, senescent human vascular endothelial cells participated in atherosclerosis via regulating the level of endothelin-1 (ET-1), nitric oxide (NO), angiotensin II and monocyte chemoattractant protein-1 (MCP-1), senescent human vascular smooth muscle cells-mediated plaque instability and vascular calcification via regulating the expression level of BMP-2, OPN, Runx-2 and inflammatory molecules, and senescent macrophages impaired cholesterol efflux and promoted the development of senescent-related cardiovascular diseases. This review summarizes the characteristics of cell senescence and updates the molecular mechanisms underlying cell senescence. Moreover, we also discuss the recent advances on the molecular mechanisms that can potentially regulate the development and progression of atherosclerosis.
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