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Mitochondrial dynamics, mitochondrial fusion and fission may be involved in myocardial ischemia/reperfusion (MI/R) injury. In particular, mitochondrial fission is associated with mitochondrial fragmentation and decreased ATP production leading to cardiac contractile dysfunction and increased infarct size in MI/R [1-3]. During ischemic events, coronary blood flow is restricted causing cardiomyocytes to enter a hypoxic state. This change in cellular respiration causes a buildup of lactic acid and a decrease in pH. The acidic conditions developed during ischemia prevent the opening of the mitochondrial permeability transition pore (MPTP) and cause cardiomyocyte hypercontracture. When blood flow and oxygen delivery are restored during reperfusion, reactive oxygen species (ROS) are generated which leads to the loss of mitochondrial membrane potential and opening of the MPTP, which potentiates mitochondrial fission in MI/R (Figure 1). Therefore inhibiting mitochondrial fission, which results from the vital act of reperfusion, may be a strategy to salvage damaged cardiomyocytes and protect them from MI/R injury. P110 (DLLPRGT) is a mitochondrial fission peptide inhibitor that acts by selectively inhibiting the interaction between human fission protein (Fis1), which is located on the outer mitochondrial membrane and dynamin related protein 1 (Drp1), a GTPase (Figure 2).

Comparison of the Effects of Myristoylated and Transactivating Peptide (TAT) Conjugated Mitochondrial Fission Peptide Inhibitor (P110) in Myocardial Ischemia/Reperfusion (I/R) Injury