Authors: Tamara P Martin, Ewan Cameron, Stuart Nicklin, Christopher M Loughrey
Published: 2020-10-27
DOI: 10.1161/res.127.suppl_1.339
Source: Full article
Myocardial infarction (MI) is a leading cause of heart failure (HF) and mortality worldwide. Preservation of contractile function and prevention of adverse cardiac remodelling following MI are essential to limit progression to HF. Expression of the Runx1 transcription factor in border zone cardiomyocytes is increased within 24 hours after MI. Genetically modified mice with Runx1 deficiency demonstrate an absence of cardiac dilation and preservation of left ventricular (LV) contractility following MI without a change of infarct size. Here, we investigate if adeno-associated viral (AAV)-mediated gene transfer to knock-down Runx1 expression post-MI attenuates adverse cardiac remodelling in mice. Male C57BL/6J mice underwent LAD ligation followed by intravenous injection of AAV-Runx1-shRNA or control AAV-scramble-shRNA (1x10