Antifibrotic therapies to control cardiac fibrosis.pdf

2019-03-04T23:39:41Z (GMT) by Jianjun Guan
Cardiac fibrosis occurs naturally after myocardial infarction. While the initially formed fibrotic tissue prevents the
infarcted heart tissue from rupture, the progression of cardiac fibrosis continuously expands the size of fibrotic
tissue and causes cardiac function decrease. Cardiac fibrosis eventually evolves the infarcted hearts into heart
failure. Inhibiting cardiac fibrosis from progressing is critical to prevent heart failure. However, there is no efficient
therapeutic approach currently available. Myofibroblasts are primarily responsible for cardiac fibrosis. They are
formed by cardiac fibroblast differentiation, fibrocyte differentiation, epithelial to mesenchymal transdifferentiation,
and endothelial to mesenchymal transition, driven by cytokines such as transforming growth factor beta (TGF-β),
angiotensin II and platelet-derived growth factor (PDGF). The approaches that inhibit myofibroblast formation
have been demonstrated to prevent cardiac fibrosis, including systemic delivery of antifibrotic drugs, localized
delivery of biomaterials, localized delivery of biomaterials and antifibrotic drugs, and localized delivery of cells
using biomaterials. This review addresses current progresses in cardiac fibrosis therapies.