This review summarizes current knowledge of how inflammatory drivers respond to molecular signals to coordinate cardiac wound healing after myocardial infarction in mouse models.
This review outlines the cellular and molecular mechanisms of cardiac wound healing after myocardial infarction in mouse models, highlighting pathways that lead to maladaptive remodeling and heart failure.
Wound healing after myocardial infarction (MI) is a dynamic and multifaceted process that links the molecular alterations induced by or in response to prolonged ischemia with structural and physiological changes to the damaged myocardium. Changes, at the tissue level, are driven by a complex intersection of cellular and molecular mechanisms that operate along a classic wound healing paradigm as an attempt to repair the damaged myocardium and restore cardiac physiology. Maladaptive healing prevents a return to the original homeostasis, rather yielding a myocardium reset to a new homeostatic status that can lead to heart failure due to compromised contractility, increased chamber dilation, and cardiac fibrosis or due to sudden cardiac death resulting from arrhythmias. This review summarizes our current knowledge of how key inflammatory drivers in the myocardium (cardiomyocytes, neutrophils, monocytes/macrophages, fibroblasts, and vascular endothelial cells) respond to molecular signals including cytokines, growth factors, and proteases to coordinate the wound healing process in the mouse model of MI. We also identify knowledge gaps that remain in our understanding of cardiac remodeling that are opportunities for future examinations.
Toba et al. (Wed,) conducted a review in Myocardial infarction. This review summarizes current knowledge of how inflammatory drivers respond to molecular signals to coordinate cardiac wound healing after myocardial infarction in mouse models.