Journal
BIOMEDICINES
Volume 9, Issue 10, Pages -Publisher
MDPI
DOI: 10.3390/biomedicines9101356
Keywords
endothelial dysfunction; gliflozins; cardiovascular diseases; heart prevention
Categories
Funding
- Programma VALERE, University of Campania Luigi Vanvitelli
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Type 2 diabetes mellitus is a known risk factor for cardiovascular disease and heart failure, making prevention of cardiovascular events crucial in managing diabetic patients. Endothelial dysfunction is an early event in atherosclerosis and plays a key role in the development of diabetes complications. SGLT2 inhibitors have shown cardiovascular benefits in diabetic patients, although the underlying mechanisms are still not fully understood.
Type 2 diabetes mellitus (T2DM) is a known independent risk factor for atherosclerotic cardiovascular disease (CVD) and solid epidemiological evidence points to heart failure (HF) as one of the most common complications of diabetes. For this reason, it is imperative to consider the prevention of CV outcomes as an effective goal for the management of diabetic patients, as important as lowering blood glucose. Endothelial dysfunction (ED) is an early event of atherosclerosis involving adhesion molecules, chemokines, and leucocytes to enhance low-density lipoprotein oxidation, platelet activation, and vascular smooth muscle cell proliferation and migration. This abnormal vascular phenotype represents an important risk factor for the genesis of any complication of diabetes, contributing to the pathogenesis of not only macrovascular disease but also microvascular damage. Gliflozins are a novel class of anti-hyperglycemic agents used for the treatment of Type 2 diabetes mellitus (T2DM) that selectively inhibit the sodium glucose transporter 2 (SGLT2) in the kidneys and have provoked large interest in scientific community due to their cardiovascular beneficial effects, whose underlying pathophysiology is still not fully understood. This review aimed to analyze the cardiovascular protective mechanisms of SGLT2 inhibition in patients T2DM and their impact on endothelial function.
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