In the diseased heart, cardiomyocytes undergo necrotic cell death. A healing response results in myofibroblast production of collagen and other matrix molecules, which initially serve to preserve the structural integrity of the myocardium. However, myofibroblast dispersion fails to occur in many cardiac diseases, and perpetual matrix formation leads to adverse remodelling of the heart. In this Review, Weber et al. discuss relevant mechanisms of cardiac fibrosis and consequent remodelling, and highlight potential strategies for cardioprotection.
- Karl T. Weber
- Yao Sun
- Ivan C. Gerling
