Upregulation of endothelial DRP1 promotes a pathological vasodilation mechanism in response to flow-induced dilation
| Autor: | Cristhian Gutierrez Huerta, Erin Birch, Shelby Hader, Amanda LeBlanc, David Guterrman, Andreas Beyer |
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| Rok vydání: | 2023 |
| Předmět: | |
| Zdroj: | Physiology. 38 |
| ISSN: | 1548-9221 1548-9213 |
| DOI: | 10.1152/physiol.2023.38.s1.5732875 |
| Popis: | Background: Endothelial microvascular dysfunction is a strong and independent risk factor for coronary artery disease (CAD), and improvements in microvascular function improve rates of survivability. Microvascular endothelium of healthy individuals releases nitric oxide (NO) in response to increased blood flow, while individuals with CAD release mitochondria-derived hydrogen peroxide (H2O2), a reactive oxygen species (ROS) molecule, in response to the same stimulus. Mitochondrial fission, a mitochondrial regulatory mechanism that is mediated by DRP1, is associated with increased ROS production as well as a multitude of cardiometabolic disease including obesity, pulmonary arterial hypertension, and diabetes. Aim: We hypothesize that increased endothelial DRP1 mediates the phenotypic shift in the release of NO to H2O2 in response to increased blood flow in individuals with CAD. Methods & Results: Atrial and adipose tissue was obtained from surgical discard tissue from individuals with and without CAD (non-CAD). Western blot analysis of LV tissue shows increased DRP1 expression in individuals with CAD compared to non-CAD (1.97 to 0.99, N=3-7, p American Physiology Society (Porter Fellowship, CG), NIH/NHLBI R01 HL-135901 (Gutterman), NIH/NHLBI R01 HL-133029 (Beyer), AHA SFRN, Medical College of Wisconsin (Beyer) This is the full abstract presented at the American Physiology Summit 2023 meeting and is only available in HTML format. There are no additional versions or additional content available for this abstract. Physiology was not involved in the peer review process. |
| Databáze: | OpenAIRE |
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