The goal of this chapter is to discuss the regulation of cardiac fibrosis by miRNAs. Cardiac myocytes
are normally surrounded by a fine network of collagen fibers. In the normal heart, two thirds of the cell
population is composed of nonmuscle cells, the majority of which are fibroblasts. Cardiac fibrosis is the result of
both an increase in fibroblast proliferation and extracellular matrix (ECM) deposition. A growing body of
evidence indicates that, along with cardiomyocytes hypertrophy, diffusion of interstitial fibrosis is a key
pathologic feature of myocardial remodelling in a number of cardiac diseases of different (e.g. ischemic,
hypertensive, valvular, genetic, and metabolic) origin. The extracellular matrix (ECM) is a dynamic
microenvironment; changes within ECM constitute the second important myocardial adaptation that occurs
during cardiac remodelling. A subset of miRNAs is enriched in cardiac fibroblasts compared to cardiomyocytes.
A number of studies have demonstrated the involvement of miRNAs in regulating myocardial fibrosis in the
settings of myocardial ischemia or mechanical overload. Some miRNAs (miR-208 and miR-21) have been shown
to favor fibrogenesis, being profibrotic miRNAs. Others including miR-29, miR-133, miR-30c, and miR-590
have been demonstrated to produce inhibitory effects on fibrogenesis, being anti-fibrotic miRNAs.
