Fibrosis as a Therapeutic Target Post-Myocardial Infarction

Title: Fibrosis as a Therapeutic Target Post-Myocardial Infarction

Volume: 11 Issue: 4

Author(s): Fiona See, Andrew Kompa, Jennifer Martin, Dion A. Lewis and Henry Krum

Affiliation:

Keywords: fibrosis, remodelling, renin-angiotensin, endothelin, transforming growth factor, collagen

Abstract: The extracellular matrix (ECM) is a dynamic microenvironment and a major contributor to the adverse ventricular remodelling that follows myocardial infarction (MI), via activation of both direct pro-fibrotic pathways and matrix metalloproteinases (MMPs) that enhance collagenase activity. Reactive fibrosis, i.e. deposition of ECM materials remote from the region of the MI is clearly detrimental to ventricular function and contributory to adverse outcomes post- MI. Therefore, reversal of this process represents an important therapeutic target in post-MI management and treatment of established heart failure. A number of existing agents exert their beneficial effects in part via reductions in ECM deposition. Furthermore, specific anti-fibrotic drugs have been developed and are currently being explored for these and other cardiac conditions where pathological ECM deposition is felt to be contributory to disease progression.

Cite this article as:

See Fiona, Kompa Andrew, Martin Jennifer, Lewis A. Dion and Krum Henry, Fibrosis as a Therapeutic Target Post-Myocardial Infarction, Current Pharmaceutical Design 2005; 11 (4) . https://dx.doi.org/10.2174/1381612053382098