| First Author | Hassink RJ | Year | 2008 |
| Journal | Cardiovasc Res | Volume | 78 |
| Issue | 1 | Pages | 18-25 |
| PubMed ID | 18079102 | Mgi Jnum | J:140281 |
| Mgi Id | MGI:3813199 | Doi | 10.1093/cvr/cvm101 |
| Citation | Hassink RJ, et al. (2008) Cardiomyocyte cell cycle activation improves cardiac function after myocardial infarction. Cardiovasc Res 78(1):18-25 |
| abstractText | AIMS: Cardiomyocyte loss is a major contributor to the decreased cardiac function observed in diseased hearts. Previous studies have shown that cardiomyocyte-restricted cyclin D2 expression resulted in sustained cell cycle activity following myocardial injury in transgenic (MHC-cycD2) mice. Here, we investigated the effects of this cell cycle activation on cardiac function following myocardial infarction (MI). METHODS AND RESULTS: MI was induced in transgenic and non-transgenic mice by left coronary artery occlusion. At 7, 60, and 180 days after MI, left ventricular pressure-volume measurements were recorded and histological analysis was performed. MI had a similar adverse effect on cardiac function in transgenic and non-transgenic mice at 7 days post-injury. No improvement in cardiac function was observed in non-transgenic mice at 60 and 180 days post-MI. In contrast, the transgenic animals exhibited a progressive and marked increase in cardiac function at subsequent time points. Improved cardiac function in the transgenic mice at 60 and 180 days post-MI correlated positively with the presence of newly formed myocardial tissue which was not apparent at 7 days post-MI. Intracellular calcium transient imaging indicated that cardiomyocytes present in the newly formed myocardium participated in a functional syncytium with the remote myocardium. CONCLUSION: These findings indicate that cardiomyocyte cell cycle activation leads to improvement of cardiac function and morphology following MI and may represent an important clinical strategy to promote myocardial regeneration. |
