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GLP-1RAs and cardiovascular disease: is the endothelium a relevant platform?

期刊

ACTA DIABETOLOGICA
卷 60, 期 11, 页码 1441-1448

出版社

SPRINGER-VERLAG ITALIA SRL
DOI: 10.1007/s00592-023-02124-w

关键词

Diabetes; GLP-1 receptor agonists; Endothelium; Atherosclerosis

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High blood sugar strongly affects endothelial function and activation, increasing the risk of atherosclerotic cardiovascular disease. Glucagon-like peptide 1 receptor agonists (GLP-1RA), a class of drugs aimed at lowering blood glucose levels, show potential in improving endothelium damage and cardiovascular disease progression. They have direct favorable actions on coronary vascular endothelium, such as reducing oxidative stress and increasing nitric oxide. Further research is needed to understand the specific role of GLP-1RA in cardiovascular disease management and identify cellular targets involved in protective signal transmission.
Hyperglycemia strongly affects endothelial function and activation, which in turn increases the risk of atherosclerotic cardiovascular disease. Among pharmacotherapies aimed at lowering blood glucose levels, glucagon-like peptide 1 receptor agonists (GLP-1RA) represent a class of drugs involved in the improvement of the endothelium damage and the progression of cardiovascular diseases. They show antihypertensive and antiatherosclerotic actions due at least in part to direct favorable actions on the coronary vascular endothelium, such as oxidative stress reduction and nitric oxide increase. However, cumulative peripheral indirect actions could also contribute to the antiatherosclerotic functions of GLP-1/GLP-1R agonists, including metabolism and gut microbiome regulation. Therefore, further research is necessary to clarify the specific role of this drug class in the management of cardiovascular disease and to identify specific cellular targets involved in the protective signal transduction. In the present review, we provide an overview of the effects of GLP-1RAs treatment on cardiovascular disease with particular attention on potential molecular mechanisms involving endothelium function on formation and progression of atherosclerotic plaque.

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