| First Author | Zhou N | Year | 2019 |
| Journal | Mol Med Rep | Volume | 20 |
| Issue | 4 | Pages | 3840-3848 |
| PubMed ID | 31485654 | Mgi Jnum | J:290111 |
| Mgi Id | MGI:6435295 | Doi | 10.3892/mmr.2019.10632 |
| Citation | Zhou N, et al. (2019) p27kip1 haploinsufficiency preserves myocardial function in the early stages of myocardial infarction via Atg5mediated autophagy flux restoration. Mol Med Rep 20(4):3840-3848 |
| abstractText | Myocardial infarction (MI) is a leading cause of mortality in adults worldwide. Over the last two decades, gene therapy has been a hot topic in cardiology, and there has been a focus on cell cycle inhibitors and their protective effects on the myocardium postMI. In our previous study, the haploinsufficiency of p27kip1 (p27) was demonstrated to improve cardiac function in mice postMI by promoting angiogenesis and myocardium protection through the secretion of growth factors. Autophagy is an adaptive response of cells to environmental changes, such as nutrient deprivation, ischemia and hypoxia. The appropriate regulation of autophagy may improve myocardial function by preventing apoptosis of cardiomyocytes. In this study, we used immunoassays, transmission electron microscopy and cardiac ultrasound to confirm that p27 haploinsufficiency prevents myocardial apoptosis by restoring autophagy protein 5mediated autophagy flux in the early stages of MI. The present study provides a novel method for studying MI or ischemic heart disease therapy. |
