Acute myocardial infarction (AMI) results from an occlusive thrombus physically blocking a coronary vessel supplying the heart with oxygenated blood. Myocardial ischaemia leads to enhanced oxidative stress and irreversible damage to the affected myocardium. In response to myocardial ischaemia, cardiac myocytes undergo a cascade of signalling events including the recruitment of inflammatory cells such as neutrophils. Activated neutrophils cause interstitial fibrosis and promote secondary cellular damage through unregulated production of potent oxidants such as hypochlorous acid (HOCl), which in turn may play a role in promoting cardiac remodelling and subsequent cardiac dysfunction. Understanding the molecular mechanisms underlying the recruitment and activation of inflammatory cells following myocardial infarction and subsequent impact of inflammatory processes on the myocardium is important due to the potential for these processes to promote heart failure. This review highlights key changes to signalling proteins subsequent to myocardial inflammation after AMI, and will focus discussion on oxidant species generated in the myocardium during inflammation and how these oxidants impact on signal transduction cascades in cardiac myocytes and finally discusses the development of inhibitors that diminish oxidant production by activated neutrophils by targeting neutrophil myeloperoxidase.
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