Abstract

Heart disease with attendant cardiac fibrosis is a chronic economic and social burden in developed countries, killing more patients in developed countries than any other disease [1]. One of the major etiologies for cardiac fibrosis includes the chronic pathology associated with post-myocardial infarction, which can lead to activation and maintenance of profibrotic myofibroblasts in the heart that persist well after expansion and activation phases to then influence the accumulation of extracellular matrix in the noninfarcted regions of the heart [2].

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