The accumulation of the antifibrotic peptide AcSDKP provides a mechanistic explanation for the blood pressure-independent organ-protective and antifibrotic benefits of ACE inhibitors compared to ARBs.
Blockade of the renin-angiotensin system (RAS) is well recognized as an essential therapy in hypertensive, heart, and kidney diseases. There are several classes of drugs that block the RAS; these drugs are known to exhibit antifibrotic action. An analysis of the molecular mechanisms of action for these drugs can reveal potential differences in their antifibrotic roles. In this review, we discuss the antifibrotic action of RAS blockade with an emphasis on the potential importance of angiotensin I-converting enzyme (ACE) inhibition associated with the antifibrotic peptide N-acetyl-seryl-aspartyl-lysyl-proline (AcSDKP).
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Kanasaki et al. (2011) studied this question.
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