| First Author | Lima B | Year | 2009 |
| Journal | Proc Natl Acad Sci U S A | Volume | 106 |
| Issue | 15 | Pages | 6297-302 |
| PubMed ID | 19325130 | Mgi Jnum | J:147758 |
| Mgi Id | MGI:3842056 | Doi | 10.1073/pnas.0901043106 |
| Citation | Lima B, et al. (2009) Endogenous S-nitrosothiols protect against myocardial injury. Proc Natl Acad Sci U S A 106(15):6297-302 |
| abstractText | Despite substantial evidence that nitric oxide (NO) and/or endogenous S-nitrosothiols (SNOs) exert protective effects in a variety of cardiovascular diseases, the molecular details are largely unknown. Here we show that following left coronary artery ligation, mice with a targeted deletion of the S-nitrosoglutathione reductase gene (GSNOR(-/-)) have reduced myocardial infarct size, preserved ventricular systolic and diastolic function, and maintained tissue oxygenation. These profound physiological effects are associated with increases in myocardial capillary density and S-nitrosylation of the transcription factor hypoxia inducible factor-1alpha (HIF-1alpha) under normoxic conditions. We further show that S-nitrosylated HIF-1alpha binds to the vascular endothelial growth factor (VEGF) gene, thus identifying a role for GSNO in angiogenesis and myocardial protection. These results suggest innovative approaches to modulate angiogenesis and preserve cardiac function. |
