Understanding the role of ACE and related peptides in post-MI wound healing provides a mechanistic basis for pharmacologic interventions to prevent adverse remodeling.
A wound-healing response that eventuates in fibrous tissue formation appears at the site of myocardial infarction (MI) in the affected ventricle. Fibrosis can likewise appear remote to the MI and cause an extensive structural remodeling of the myocardium of infarcted and noninfarcted ventricles. Substances involved in promoting healing at and remote to MI are of considerable interest and an important clinical issue, given that the healing response is subject to pharmacologic intervention. Angiotensin-converting enzyme (ACE) is expressed by wound-healing fibroblast-like cells; it likely serves to regulate local concentrations of angiotensin II and bradykinin involved in healing and matrix remodeling. Wound healing following MI and its regulation are addressed in this review.
Weber et al. (Sat,) studied this question.
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