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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
 

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Angiotensin-converting enzyme 2 is an essential regulator of heart function.

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.[1]

References

  1. Angiotensin-converting enzyme 2 is an essential regulator of heart function. Crackower, M.A., Sarao, R., Oudit, G.Y., Yagil, C., Kozieradzki, I., Scanga, S.E., Oliveira-dos-Santos, A.J., da Costa, J., Zhang, L., Pei, Y., Scholey, J., Ferrario, C.M., Manoukian, A.S., Chappell, M.C., Backx, P.H., Yagil, Y., Penninger, J.M. Nature (2002) [Pubmed]
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