Kruppel-Like Factor 14 Improves Cardiac Function After Myocardial Infarction

Abstract

BackgroundReversal of heart failure after myocardial infarction (MI) remains a global challenge. The goal of a clinical physician is to prevent heart failure immediately following the infarct. Since traditional strategies are only partially helpful for improving cardiac function, there is an urgency to identify novel approaches to maintain cardiac function. ObjectivesThe aim of this study was to determine the role of Kruppel-Like Factor 14 (KLF14) in the heart post-MI. Methods and ResultsWild-type and KLF14 overexpression mice were subjected to MI. At four weeks following MI, the infarct size was significantly reduced, left ventricular fraction shortening was significantly preserved, and left ventricular chamber dilation was attenuated in the KLF14 overexpression group. Transmission electron microscopy studies revealed striking evidence of decreased mitochondrial damage in the KLF14 overexpression myocardium following MI. To gain insight into the underlying relationship between KLF14 and mitochondria, we examined a broad array of genes involved in mitochondrial function and found that KLF14 overexpression was involved in the decreased apoptosis of mitochondria induced by H2O2. This beneficial effect was associated with increased levels of PGC-1. ConclusionsThese results demonstrate that KLF14 plays a critical protective role in the heart after MI by regulating mitochondrial function, which may be achieved by regulating PGC-1.