Key result
Nrf2 protects endothelial function and slows atherosclerosis by curbing oxidative stress and mitochondrial damage.
Why the study?
The specific mechanisms by which Nrf2 reduces cardiovascular disease remain unknown.
Targeting the Nrf2-ARE signaling pathway represents a potential novel therapeutic approach to protect against endothelial dysfunction and atherosclerosis.
Nrf2 activation may protect endothelium in atherosclerosis; leaves open clinical translation amid conflicting animal data.
Cardiovascular disease (CVD) is a serious public health issue in China, accounting for more than 40% of all mortality, and it is the leading cause of death worldwide. Atherosclerosis is the pathological basis for much CVD, including coronary heart disease, acute myocardial infarction, and stroke. Endothelial dysfunction is an initiating and exacerbating factor in atherosclerosis. Recent research has linked oxidative stress and mitochondrial damage to endothelial dysfunction. Nuclear factor erythroid 2-related factor 2 (Nrf2) is a transcription factor with antioxidant effects that is strongly connected to several CVDs. However, the mechanism by which Nrf2 reduces CVD is unknown. Research indicates that Nrf2 improves endothelial function by resisting oxidative stress and mitochondrial damage, thereby delaying atherosclerosis. This article examines the mechanisms and potential targets of Nrf2 affecting endothelial cell function to improve atherosclerosis and to provide ideas for the development of new CVD treatments.
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Huang et al. (2022) conducted a review in Atherosclerosis. Nrf2 was evaluated. Nrf2 improves endothelial function by resisting oxidative stress and mitochondrial damage, thereby delaying atherosclerosis.
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