Key result
TET2 regulates vascular cell dysfunction and inflammation, emerging as a potential target in atherosclerosis.
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Atherosclerosis is the underlying cause of cardio-cerebrovascular disease. However, the mechanisms of atherosclerosis are still unclear. The modification of DNA methylation has an important role in atherosclerosis development. As a member of the Ten-eleven translocation (TET) family, TET methylcytosine dioxygenase 2 (TET2) can modify DNA methylation by catalyzing 5-methylcytosine to 5-hydroxymethylcytosine and mediate DNA demethylation. Recent findings suggest that TET2 is related to the phenotype transformation of vascular smooth muscle cells, endothelial dysfunction, and inflammation of macrophage, the key factors of atherosclerosis. Therefore, TET2 may be a potential target for atherosclerosis treatment. This review will elaborate the recent findings that suggest the role of TET2 in atherosclerosis.
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Liu et al. (2018) conducted a review in Atherosclerosis. TET methylcytosine dioxygenase 2 (TET2) was evaluated. TET2 modifies DNA methylation and regulates vascular smooth muscle cell transformation, endothelial dysfunction, and macrophage inflammation, making it a potential target for atherosclerosis.
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