10.25376/hra.7800977.v1 Jianjun Guan Jianjun Guan Antifibrotic therapies to control cardiac fibrosis.pdf Health Research Alliance 2019 Myocardial Infarction/prevention & control Cardiac fibrosis myofibroblasts anti-fibrotic therapeutics Biomaterials Biomedical Engineering not elsewhere classified 2019-03-04 23:39:41 Journal contribution https://hra.figshare.com/articles/journal_contribution/Antifibrotic_therapies_to_control_cardiac_fibrosis_pdf/7800977 <div>Cardiac fibrosis occurs naturally after myocardial infarction. While the initially formed fibrotic tissue prevents the</div><div>infarcted heart tissue from rupture, the progression of cardiac fibrosis continuously expands the size of fibrotic</div><div>tissue and causes cardiac function decrease. Cardiac fibrosis eventually evolves the infarcted hearts into heart</div><div>failure. Inhibiting cardiac fibrosis from progressing is critical to prevent heart failure. However, there is no efficient</div><div>therapeutic approach currently available. Myofibroblasts are primarily responsible for cardiac fibrosis. They are</div><div>formed by cardiac fibroblast differentiation, fibrocyte differentiation, epithelial to mesenchymal transdifferentiation,</div><div>and endothelial to mesenchymal transition, driven by cytokines such as transforming growth factor beta (TGF-β),</div><div>angiotensin II and platelet-derived growth factor (PDGF). The approaches that inhibit myofibroblast formation</div><div>have been demonstrated to prevent cardiac fibrosis, including systemic delivery of antifibrotic drugs, localized</div><div>delivery of biomaterials, localized delivery of biomaterials and antifibrotic drugs, and localized delivery of cells</div><div>using biomaterials. This review addresses current progresses in cardiac fibrosis therapies.</div>