Cardiac
fibrosis is associated with non-ischemic
dilated cardiomyopathy, increasing its morbidity and mortality. Cardiac fibroblast is the keystone of fibrogenesis, being activated by numerous cellular and humoral factors. Macrophages, CD4+ and CD8+ T cells, mast cells, and endothelial cells stimulate fibrogenesis directly by activating cardiac fibroblasts and indirectly by synthetizing various profibrotic molecules. The synthesis of type 1 and type 3
collagen,
fibronectin, and α-smooth muscle actin is rendered by various mechanisms like
transforming growth factor-beta/small mothers against decapentaplegic pathway, renin angiotensin system, and
estrogens, which in turn alter the extracellular matrix. Investigating the underlying mechanisms will allow the development of diagnostic and prognostic tools and discover novel specific
therapies. Serum
biomarkers aid in the diagnosis and tracking of cardiac
fibrosis progression. The diagnostic gold standard is cardiac magnetic resonance with
gadolinium administration that allows quantification of cardiac
fibrosis either by late
gadolinium enhancement assessment or by T1 mapping. Therefore, the goal is to stop and even reverse cardiac
fibrosis by developing specific
therapies that directly target fibrogenesis, in addition to the drugs used to treat
heart failure.
Cardiac resynchronization therapy had shown to revert myocardial remodeling and to reduce cardiac
fibrosis. The purpose of this review is to provide an overview of currently available data.