The regulation of inflammation in ventricular remodelling after myocardial infarction

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Heart failure (HF) is when the heart is unable to pump with enough force to meet the demands of the body. It frequently results from a heart attack (myocardial infarction or MI) causing impaired heart function. Despite current treatments, HF after MI causes significant morbidity and mortality. Inflammation, the body's response to harmful stimuli that is largely mediated by circulating white blood cells, is an important response to MI. However, there is compelling evidence implicating excessive inflammation in the development of post-MI HF. Certain types of inflammatory cells, called monocytes and macrophages, appear especially important. Blocking the influx of monocytes and macrophages after MI may prevent HF. This project aims to study the behaviour and molecular signalling of these cells after MI by manipulating a molecule called Nrf2, which is known to mitigate inflammation after a heart attack. It is hoped that these studies will identify new treatment targets with the ultimate aim of developing new ways of treating patients after MI to alleviate the development of HF.