Key result
Reversal of reactive fibrosis and extracellular matrix deposition represents an important therapeutic target in post-myocardial infarction management and heart failure.
Targeting reactive fibrosis and extracellular matrix deposition is a promising therapeutic strategy to prevent adverse ventricular remodeling post-myocardial infarction.
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Supports targeting fibrosis post-MI; leaves open prospective validation of anti-fibrotic therapies.
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.
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See et al. (2005) conducted a review in Myocardial infarction and heart failure. Anti-fibrotic drugs was evaluated. Reversal of reactive fibrosis and extracellular matrix deposition represents an important therapeutic target in post-myocardial infarction management and heart failure.
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