Following myocardial infarction (MI), a dynamic and complex process called wound healing is initiated, aiming to produce a
robust scar and limit adverse remodeling of the left ventricle (LV). Cardiac fibroblasts (CFs) - the most populous cardiac cell-type - differentiate
into myofibroblasts under the influence of post-MI mechanical stress, transforming growth factor β (TGF-β) and various inflammatory
signals. Myofibroblasts are contractile cells that start producing extracellular matrix (ECM) components and secrete factors
that orchestrate wound healing, but also promote adverse cardiac remodeling that can progress to life-threatening heart failure (HF). Due
to their vital role in the wound healing and LV remodeling after MI, (myo)fibroblasts have been receiving more and more attention lately
as targets for anti-HF treatment strategies. In this review, we will summarize the current knowledge regarding the cardiac (myo)fibroblast
characteristics, discuss the signaling pathways and the factors that affect their migration, proliferation and differentiation post-MI, as well
as their ECM-depositing capabilities. Finally, we will provide an overview of the latest innovative research that is targeting the
(myo)fibroblast, in an attempt to limit adverse remodeling and prevent HF.
Keywords: Fibroblast, myofibroblast, myocardial infarction, heart, cardiac remodeling, heart failure.
Rights & PermissionsPrintExport