Runx1 deficiency protects against cardiac ischaemia-reperfusion injury in ex vivo mouse hearts

Abstract

Background: Acute coronary artery occlusion resulting in myocardial ischaemia leads to cardiomyocyte death and contractile dysfunction. Restoration of the coronary circulation is imperative to limit cell death and salvage viable tissue but also causes paradoxical cell injury. Previous work showed that expression of the transcription factor Runx1 is increased in cardiomyocytes at one day post-myocardial infarction (MI) and mice with cardiomyocyte-specific Runx1 deficiency (Runx1∆/∆) have preserved left ventricular systolic function following both MI and ischemia-reperfusion (I/R) injury in vivo. However, in the absence of systemic factors the extent to which Runx1 expression can be triggered and whether Runx1∆/∆ hearts are protected against I/R injury is unknown.