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Here, we discussed various mechanisms hypothesized in previous animal and preclinical human studies, including blockade of the production of adhesion molecules and inflammatory factors, induction of endothelial cells synthesis of nitric oxide, protection of mitochondrial function and restriction of oxidative stress, suppression of NOD-like receptor thermal protein domain associated protein three inflammasome, reduction of foam cell formation and macrophage inflammation, and amelioration of vascular smooth muscle cell dysfunction, to help explain the cardiovascular benefits of GLP-1RAs in CVOTs
Glucose-6-phosphate dehydrogenase deficiency Peer reviewed by Dr Colin Tidy, MRCGPLast updated by Dr Philippa Vincent, MRCGPLast updated 6 Aug 2024 DownloadDownload Share Language Discussion Audio Version Add to preferred sources on Google Medical Professionals Professional Reference articles are designed for health professionals to use
