FIGURE 1.

Mitochondrial fission and fusion proteins as targets for cardioprotection. Mitochondrial fission induced by acute myocardial ischaemia/reperfusion injury can be targeted by mdivi‐1 and Drpitor, pharmacological inhibitors of Drp1 and P110, a peptide inhibitor of the interaction between Drp1 and hFis1 to confer cardioprotection. A number of other factors (such as SB203580, PKA activators, succinate, erythropoietin and melatonin) have also been shown to confer cardioprotection by targeting the fusion and fission proteins. Inset upper box: This scheme shows the mitochondrial fission machinery, comprising Drp1 and its outer mitochondrial membrane receptors, MiD49/MiD51, Mff and hFis1. Pre‐constriction by the endoplasmic reticulum (ER) via INF2, actin and Spire1C initiates the Drp1‐driven mitochondrial fission process. Inset lower box: This scheme shows the pleiotropic non‐fusion effect of Mfn2 in tethering mitochondria to the ER