Cardiac (myo)fibroblast: Novel Strategies for its Targeting Following Myocardial Infarction

Evangelos P. Daskalopoulos, Kevin C. M. Hermans, Matthijs Blankesteijn*

*Corresponding author for this work

Research output: Contribution to journalArticleAcademicpeer-review


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 beta (TGF-beta) 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.
Original languageEnglish
Pages (from-to)1987-2002
JournalCurrent Pharmaceutical Design
Issue number12
Publication statusPublished - Apr 2014


  • Fibroblast
  • myofibroblast
  • myocardial infarction
  • heart
  • cardiac remodeling
  • heart failure

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