| First Author | Zou Y | Year | 2003 |
| Journal | Circulation | Volume | 108 |
| Issue | 24 | Pages | 3024-30 |
| PubMed ID | 14623809 | Mgi Jnum | J:131910 |
| Mgi Id | MGI:3774808 | Doi | 10.1161/01.CIR.0000101923.54751.77 |
| Citation | Zou Y, et al. (2003) Heat shock transcription factor 1 protects cardiomyocytes from ischemia/reperfusion injury. Circulation 108(24):3024-30 |
| abstractText | BACKGROUND: Because cardiomyocyte death causes heart failure, it is important to find the molecules that protect cardiomyocytes from death. The death trap is a useful method to identify cell-protective genes. METHODS AND RESULTS: In this study, we isolated the heat shock transcription factor 1 (HSF1) as a protective molecule by the death trap method. Cell death induced by hydrogen peroxide was prevented by overexpression of HSF1 in COS7 cells. Thermal preconditioning at 42 degrees C for 60 minutes activated HSF1, which played a critical role in survival of cardiomyocytes from oxidative stress. In the heart of transgenic mice overexpressing a constitutively active form of HSF1, ischemia followed by reperfusion-induced ST-segment elevation in ECG was recovered faster, infarct size was smaller, and cardiomyocyte death was less than wild-type mice. Protein kinase B/Akt was more strongly activated, whereas Jun N-terminal kinase and caspase 3 were less activated in transgenic hearts than wild-type ones. CONCLUSIONS: These results suggest that HSF1 protects cardiomyocytes from death at least in part through activation of Akt and inactivation of Jun N-terminal kinase and caspase 3. |
