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Numerous studies have shown that dysfunction or decreased numbers of Tregs may be involved in inflammatory cardiovascular diseases (CVDs) such as atherosclerosis, hypertension, myocardial infarction, myocarditis, cardiomyopathy, valvular heart diseases, heart failure, and abdominal aortic aneurysm. Tregs can help to ameliorate CVDs by suppressing excessive inflammation through various mechanisms, including inhibition of T cells and B cells, inhibition of macrophage\u2010induced inflammation, inhibition of dendritic cells and foam cell formation, and induction of anti\u2010inflammatory macrophages. Enhancing or restoring the immunosuppressive activity of Tregs may thus serve as a fundamental immunotherapy to treat hypertension and CVDs. However, the precise molecular mechanisms underlying the Tregs\u2010induced protection against hypertension and CVDs remain to be investigated. This review focuses on recent advances in our understanding of Tregs subsets and function in CVDs. 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