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Research advance of Nrf2 on atherosclerosis by regulating vascular smooth muscle cell / 浙江大学学报·医学版
Article in English | WPRIM (Western Pacific) | ID: wpr-888500
Responsible library: WPRO
ABSTRACT
Atherosclerosis is a common pathological change in cardiovascular disease. Vascular smooth muscle cell is the main source of plaque cell and extracellular matrix, and nuclear factor-erythroid 2-related factor 2 (Nrf2) is a key transcription factor regulating the function of vascular smooth muscle cell. In the process of atherosclerosis, Nrf2 signaling pathway has the following regulatory effects on vascular smooth muscle cell regulating the phenotype of vascular smooth muscle cell to change to the direction conducive to the alleviation of disease progression; inhibiting the proliferation and migration of vascular smooth muscle cell; mitigating the level of blood lipid; alleviating vascular smooth muscle cell calcification, aging and apoptosis process. This article reviews the specific mechanisms of Nrf2 regulating atherosclerosis, such as phenotypic transformation, proliferation and migration, lipid metabolism, calcification, aging and apoptosis in atherosclerosis, in order to provide a basis for understanding the molecular mechanism of atherosclerosis development and finding therapeutic targets.
Subject(s)

Full text: Available Database: WPRIM (Western Pacific) Main subject: Signal Transduction / Cell Movement / Cells, Cultured / Myocytes, Smooth Muscle / Cell Proliferation / Atherosclerosis / NF-E2-Related Factor 2 / Muscle, Smooth, Vascular Limits: Humans Language: English Journal: Journal of Zhejiang University. Medical sciences Year: 2021 Document type: Article
Full text: Available Database: WPRIM (Western Pacific) Main subject: Signal Transduction / Cell Movement / Cells, Cultured / Myocytes, Smooth Muscle / Cell Proliferation / Atherosclerosis / NF-E2-Related Factor 2 / Muscle, Smooth, Vascular Limits: Humans Language: English Journal: Journal of Zhejiang University. Medical sciences Year: 2021 Document type: Article
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