Mitochondrial cardiolipin and other structural changes mediating cardiac dysfunction in the reperfused myocardium

Reperfusion following a period of ischaemia contributes to irreversible myocardial degradation, termed ischaemia-reperfusion (IR) injury. Mitochondria are central mediators of IR injury and thus represent a key therapeutic target for preserving cardiac function. The lack of mitochondria-targeted treatment options has limited clinical efforts to rescue the reperfused myocardium and prevent post-infarction mortality. In this review, we revisit the mitochondrial structure-function relationship and the importance of the phospholipid cardiolipin in IR-induced myocardial injury. Furthermore, we consider the therapeutic potential of elamipretide, a mitochondrial inner membrane and cardiolipin-targeting peptide, highlighting its well-established long-term safety and efficacy in mitochondrial pathologies. Lastly, we summarise emerging evidence for elamipretides potential to mitigate IR injury and rescue function in the reperfused myocardium.