Key result
Targeting cardiac myofibroblasts post-MI shows promise to limit adverse LV remodeling and prevent HF.
Why the study?
Cardiac (myo)fibroblasts play a vital role in wound healing and left ventricular remodeling after myocardial infarction, but strategies to target them to limit adverse remodeling and prevent heart failure require summarization.
This review summarizes current knowledge on cardiac (myo)fibroblasts and highlights innovative research targeting these cells to limit adverse remodeling and prevent heart failure post-myocardial infarction.
May inform post-MI remodeling therapies targeting CFs; leaves open clinical translation pending prospective trials.
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.
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Daskalopoulos et al. (2014) conducted a review in Myocardial Infarction. Cardiac (myo)fibroblast targeting was evaluated. Targeting cardiac (myo)fibroblasts following myocardial infarction represents a promising strategy to limit adverse left ventricular remodeling and prevent the progression to heart failure.
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