Cardiac fibrosis, characterized by excessive deposition of extracellular matrix (ECM) proteins in the myocardium, distorts the architecture of the myocardium, facilitates the progression of arrhythmia and cardiac dysfunction, and influences the clinical course and outcome in patients with heart failure.
While adequate production of extracellular matrix (ECM) proteins is necessary for post-injury wound healing, excessive synthesis and accumulation of extracellular matrix protein in the stressed or injured hearts causes decreased or loss of lusitropy that leads to cardiac failure.
Fibroblasts play a pivotal role in cardiac remodeling and the development of heart failure through the deposition of extra-cellular matrix (ECM) proteins and also by affecting cardiomyocyte growth and function.