Cardiovascular effects of GLP-1 receptor agonism.
| Autor: | Winquist RJ; Alkermes Pharmaceuticals Inc., Waltham, MA, United States. Electronic address: winquist@aol.com., Gribkoff VK; Section on Endocrinology, Department of Internal Medicine, Yale University School of Medicine, New Haven, CT, United States; TheraStat LLC, Weston, MA, United States. |
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| Jazyk: | angličtina |
| Zdroj: | Advances in pharmacology (San Diego, Calif.) [Adv Pharmacol] 2022; Vol. 94, pp. 213-254. Date of Electronic Publication: 2022 Mar 30. |
| DOI: | 10.1016/bs.apha.2022.02.005 |
| Abstrakt: | Glucagon-like peptide-1 (GLP-1) receptor agonists are extensively used in type 2 diabetic patients for the effective control of hyperglycemia. It is now clear from outcomes trials that this class of drugs offers important additional benefits to these patients due to reducing the risk of developing major adverse cardiac events (MACE). This risk reduction is, in part, due to effective glycemic control in patients; however, the various outcomes trials, further validated by subsequent meta-analysis of the outcomes trials, suggest that the risk reduction in MACE is also dependent on glycemic-independent mechanisms operant in cardiovascular tissues. These glycemic-independent mechanisms are likely mediated by GLP-1 receptors found throughout the cardiovascular system and by the complex signaling cascades triggered by the binding of agonists to the G-protein coupled receptors. This heterogeneity of signaling pathways underlying different downstream effects of GLP-1 agonists, and the discovery of biased agonists favoring specific signaling pathways, may have import in the future treatment of MACE in these patients. We review the evidence supporting the glycemic-independent evidence for risk reduction of MACE by the GLP-1 receptor agonists and highlight the putative mechanisms underlying these benefits. We also comment on the different signaling pathways which appear important for mediating these effects. Competing Interests: Conflict of interest statement The authors declare no conflicts of interest. All data reported in the present review are from the public scientific literature. (Copyright © 2022 Elsevier Inc. All rights reserved.) |
| Databáze: | MEDLINE |
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