The present invention relates generally to a method of therapeutically or prophylactically treating ischaemia-induced myocardial tissue damage, in particular ischaemia-reperfusion-induced myocardial tissue damage. More particularly, the present invention relates to a method of reducing the extent of ischaemia-induced myocardial tissue damage in a mammal by selectively upregulating FPR1-mediated ERK signalling. The method of the present invention is useful, inter alia, in reducing the extent and/or severity of myocardial tissue damage associated with conditions characterised by myocardial ischaemia or myocardial ischaemia and reperfusion, such as acute myocardial infarction caused by atherosclerotic artery occlusion or blood clot-induced artery occlusion.
