| First Author | Zhang S | Year | 2017 |
| Journal | Cell Death Dis | Volume | 8 |
| Issue | 2 | Pages | e2586 |
| PubMed ID | 28151473 | Mgi Jnum | J:301783 |
| Mgi Id | MGI:6506915 | Doi | 10.1038/cddis.2017.17 |
| Citation | Zhang S, et al. (2017) Knockout of Eva1a leads to rapid development of heart failure by impairing autophagy. Cell Death Dis 8(2):e2586 |
| abstractText | EVA1A (Eva-1 homologue A) is a novel lysosome and endoplasmic reticulum-associated protein that can regulate cell autophagy and apoptosis. Eva1a is expressed in the myocardium, but its function in myocytes has not yet been investigated. Therefore, we generated inducible, cardiomyocyte-specific Eva1a knockout mice with an aim to determine the role of Eva1a in cardiac remodelling in the adult heart. Data from experiments showed that loss of Eva1a in the adult heart increased cardiac fibrosis, promoted cardiac hypertrophy, and led to cardiomyopathy and death. Further investigation suggested that this effect was associated with impaired autophagy and increased apoptosis in Eva1a knockout hearts. Moreover, knockout of Eva1a activated Mtor signalling and the subsequent inhibition of autophagy. In addition, Eva1a knockout hearts showed disorganized sarcomere structure and mitochondrial misalignment and aggregation, leading to the lack of ATP generation. Collectively, these data demonstrated that Eva1a improves cardiac function and inhibits cardiac hypertrophy and fibrosis by increasing autophagy. In conclusion, our results demonstrated that Eva1a may have an important role in maintaining cardiac homeostasis. |
