Abstract
Adult mammalian cardiomyocytes demonstrate scarce cycling and even lower proliferation rates in response to injury. Signals that enhance cardiomyocyte proliferation after injury will be groundbreaking, address unmet clinical needs, and represent new strategies to treat cardiovascular diseases. In vivo methods to monitor cardiomyocyte proliferation are critical to addressing this challenge. Fortunately, advances in transgenic approaches provide sophisticated techniques to quantify cardiomyocyte cycling and proliferation.
Highlights
Adult mammalian cardiomyocytes, the muscle cells of the heart, have limited ability to re-enter the cell cycle and even lower rates of division to produce new cardiomyocytes
Cardiomyocytes are lost during myocardial infarctions even with successful reperfusion, and this loss contributes to adverse left ventricular remodeling, ischemic cardiomyopathy, heart failure, arrhythmia, and death
FDA-approved medications to treat heart failure fall within a few classes designed to dampen the adrenergic or renin-angiotensin signaling systems (e.g., ACE inhibitors, ARBs) [2]
Summary
The muscle cells of the heart, have limited ability to re-enter the cell cycle and even lower rates of division to produce new cardiomyocytes. The inability of adult cardiomyocytes to cycle and proliferate significantly impacts myocardial responses to injuries. Cardiomyocytes are lost during myocardial infarctions even with successful reperfusion, and this loss contributes to adverse left ventricular remodeling, ischemic cardiomyopathy, heart failure, arrhythmia, and death. There are no reliable therapies available to replace the cardiomyocytes lost to myocardial infarction. Identifying the drugs that enhance cardiomyocyte proliferation after injury will be groundbreaking, address unmet clinical needs, and represent new strategies to treat cardiovascular diseases. Methods are needed to quantify adult cardiomyocyte cycling and replication accurately [3]. Rigorous practices are fundamental to investigate the mechanisms that prevent cycling events under conditions of normal growth, aging, and response to injury, and establish new therapies that may enhance cardiomyocyte cycling to improve myocardial function. We will review the in vivo methods to monitor cardiomyocyte proliferation, focusing on transgenic mice
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