During cardiac reperfusion after myocardial infarct The guts are vulnerable to cascading rounds of ischaemia reperfusion damage during cardiac reperfusion following a myocardial infarction (IRI) Myocardial dysfunction occurs in patients who have this injury, which leads to myocardial necrobiosis, which increases morbidity and death. New tailored treatments are needed to protect the myocardium from this damage and improve patient outcomes. The opening of the mitochondrial permeability transition pore has been identified as one of the most important sites contributing to this injury after extensive research into the role of mitochondria during ischaemia and reperfusion. This hole opens during reperfusion, producing mitochondrial expansion and dysfunction, as well as fostering apoptotic necrobiosis. Glycogen synthase kinase-3 suppression, uncoupling proteins, and mitochondrial ATP-sensitive potassium channels (mitoKATP) (GSK3). This review will summarise what has been discovered so far about statins and their cardioprotective effects on mitochondria during myocardial IRI.