MFN1 and myocardial infarction: In addition, the hearts of adult mice with combined acute ablation of both Mfn1 and Mfn2, despite apparent mitochondrial dysfunction, were protected from in vivo acute MI and IRI; in particular, the cardioprotective phenotype of Mfn1 and Mfn2 depletion was due to beneficial effects on mitochondrial Ca2+ levels, oxidative stress, and mPTP opening [146, 149].