Abstract
Following myocardial infarction, wound healing takes place in the infarct area where the non-viable cardiac tissue is replaced by a scar. Inadequate wound healing or insufficient maintenance of the extracellular matrix in the scar can lead to excessive dilatation of the ventricles, one of the hallmarks of congestive heart failure. Therefore, it is important to better understand the wound-healing process in the heart and to develop new therapeutic agents that target the infarct area in order to maintain an adequate cardiac function. One of these potential novel therapeutic targets is Wnt signaling. Wnt signaling plays an important role in embryonic myocardial development but in the adult heart the pathway is thought to be silent. However, there is increasing evidence that components of the Wnt pathway are re-expressed during cardiac repair, implying a regulatory role. Recently, several studies have been published where the effect of interventions in Wnt signaling on infarct healing has been studied. In this review, we will summarize the results of these studies and discuss the effects of these interventions on the different cell types that are involved in the wound healing process.
Highlights
Cardiovascular diseases (CVDs) are the leading causes of mortality worldwide
The wound-healing phase is a critical process for the clinical outcome of patients who have suffered from Myocardial infarction (MI)
The Wnt/Frizzled pathway is involved in many aspects of cardiac repair following MI and may be a promising therapeutic site for interventions
Summary
Cardiovascular diseases (CVDs) are the leading causes of mortality worldwide. More people die from CVDs than from any other disease. The acellular scarring was suppressed in sFRP-4 treated hearts, resulting in a better infarct healing [63] These studies implicate that sFRPs play an important role in infarct healing and this is probably by the modulating effect between Wnt ligands and Frizzled receptors and by other inhibitory or stimulating properties (for example on BMP-1). In vitro overexpression of β-catenin in cardiomyocytes and cardiac fibroblasts of rat origin resulted in reduced apoptosis It enhanced vascular endothelial growth factor (VEGF) expression in both cell types and increased α-SMA expression in fibroblasts. This suggests that resident precursor cells contribute to the endogenous regeneration of cardiac tissue in LV remodeling following MI and that this is amplified by downregulation of β-catenin The latter two studies intervene at different sites in the myocardium (depletion of βcatenin in viable cardiomyocytes versus injection in infarcted area), which may explain the discrepancy. These data show that modification of Wnt/Frizzled signaling can contribute to the actions of stem cells during cardiac repair
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