The regulation of inflammation in ventricular remodelling after myocardial infarction

心力衰竭(HF)是指心脏不能以足够的力量泵入以满足身体需求的情况。它通常是由心脏病发作(心肌梗死或MI)导致心脏功能受损引起的。尽管目前的治疗方法不同，心梗后心衰仍会导致严重的发病率和死亡率。炎症是人体对有害刺激的反应，主要由循环中的白细胞介导，是对MI的一种重要反应。然而，有令人信服的证据表明，在心肌梗塞后心力衰竭的发展过程中存在过度炎症。某些类型的炎性细胞，称为单核细胞和巨噬细胞，似乎特别重要。阻断心肌梗死后单核细胞和巨噬细胞的内流可能预防心力衰竭。该项目旨在通过操纵一种名为Nrf2的分子来研究MI后这些细胞的行为和分子信号，Nrf2已知可以减轻心脏病发作后的炎症。希望这些研究将确定新的治疗目标，最终目的是开发治疗心肌梗死后患者的新方法，以缓解心力衰竭的发展。

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.