| First Author | Crackower MA | Year | 2002 |
| Journal | Nature | Volume | 417 |
| Issue | 6891 | Pages | 822-8 |
| PubMed ID | 12075344 | Mgi Jnum | J:77232 |
| Mgi Id | MGI:2181229 | Doi | 10.1038/nature00786 |
| Citation | Crackower MA, et al. (2002) Angiotensin-converting enzyme 2 is an essential regulator of heart function. Nature 417(6891):822-8 |
| abstractText | Cardiovascular diseases are predicted to be the most common cause of death worldwide by 2020. Here we show that angiotensin-converting enzyme 2 (ace2) maps to a defined quantitative trait locus (QTL) on the X chromosome in three different rat models of hypertension. In all hypertensive rat strains, ACE2 messenger RNA and protein expression were markedly reduced, suggesting that ace2 is a candidate gene for this QTL. Targeted disruption of ACE2 in mice results in a severe cardiac contractility defect, increased angiotensin II levels, and upregulation of hypoxia-induced genes in the heart. Genetic ablation of ACE on an ACE2 mutant background completely rescues the cardiac phenotype. But disruption of ACER, a Drosophila ACE2 homologue, results in a severe defect of heart morphogenesis. These genetic data for ACE2 show that it is an essential regulator of heart function in vivo. |
