Modulation of the renin-angiotensin system (RAS), and particularly inhibition of angiotensin-converting
enzyme (ACE), a zinc metallopeptidase, has long been a prime strategy in the treatment
of hypertension. However, other angiotensin metabolites are gaining in importance
as our understanding of the RAS increases. Recently, genomic approaches have identified
the first human homologue of ACE, termed ACEH (or ACE2). ACEH differs in specificity
and physiological roles from ACE, which opens a potential new area for discovery biology.
The gene that encodes collectrin, a homologue of ACEH, is upregulated in response
to renal injury. Collectrin lacks a catalytic domain, which indicates that there is
more to ACE-like function than simple peptide hydrolysis.