MFN2 and ischemia: In a previous study, Mfn2 knockout mice exhibited mitochondrial fragmentation, which resulted in the reduction in the mitochondrial permeability transition pore(MPTP) and aggravated the mitochondrial dysfunction caused by ROS; another study showed that ischemia–reperfusion injury resulted in the low expression of the Mfn2, which resulted in mitochondrial and cardiac dysfunction [28].