Abstract
Cardiac fibrosis has been implicated in a wide variety of cardiovascular diseases. A key hallmark of pathological cardiac fibrosis is the transition of cardiac fibroblasts to myofibroblasts. This results in the excessive deposition of extracellular matrix proteins such as collagen 1 and 3. Myofibroblast activation is principally initiated by TGF-β signalling, but more recently increased tensile strength has also been implicated in this process. Reversing the myofibroblast phenotype offers a mechanism to reduce the burden of cardiac fibrosis and restore cardiac function.
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