| Full text | |
| Author(s): |
Total Authors: 4
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| Affiliation: | [1] Univ Sao Paulo, Ribeirao Preto Med Sch, Dept Pharmacol, BR-14049900 Ribeirao Preto, SP - Brazil
[2] Hoshi Univ, Inst Med Chem, Dept Physiol & Morphol, Shinagawa Ku, Tokyo - Japan
Total Affiliations: 2
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| Document type: | Review article |
| Source: | BASIC & CLINICAL PHARMACOLOGY & TOXICOLOGY; v. 123, n. 5, p. 523-538, NOV 2018. |
| Web of Science Citations: | 6 |
| Abstract | |
Diabetes currently affects more than 400 million people worldwide. This metabolic disorder causes various micro- and macrovascular complications that accelerate atherosclerosis and yet trigger other cardiovascular diseases. The characteristic frame of hyperglycaemia, hyperinsulinaemia and hyperlipidaemia in diabetes increases several inflammatory mediators leading to endothelial dysfunction and pro-atherosclerotic processes. This MiniReview summarizes evidence that antidiabetic drugs have effects beyond lowering glycaemic levels. In experimental studies, antidiabetic drugs reduce the vascular production and release of pro-inflammatory cytokines, the recruitment, infiltration and activation of immune cells and pro-inflammatory mediators, thus decreasing vascular inflammatory responses; they also re-establish vascular redox homeostasis by reducing oxidative stress and balancing the release of vasoconstrictor and vasodilator factors, hence contributing to the improvement of endothelial function. These effects are associated with a reduction in vascular remodelling due to decreased matrix metalloproteinases expression/activity, reduced inflammatory processes and vascular wall fibrosis. In clinical studies, antidiabetic drugs also reduce the production and release of pro-inflammatory, pro-atherosclerotic and pro-oxidative mediators and improve flow-mediated dilatation, indicating beneficial effects on endothelial function. These bonus effects of antidiabetic drugs may delay and/or reduce the installation and development of the atherosclerotic disease, decrease cardiovascular risk and possibly impact mortality risk, life expectancy and quality. (AU) | |
| FAPESP's process: | 13/08216-2 - CRID - Center for Research in Inflammatory Diseases |
| Grantee: | Fernando de Queiroz Cunha |
| Support Opportunities: | Research Grants - Research, Innovation and Dissemination Centers - RIDC |