biostudies-literaturePapanicolaou KNNIA NIH HHSNHLBI NIH HHS1309-28https://www.ebi.ac.uk/biostudies/studies/S-EPMC3067905biostudies-literatureUnknown31(6)Mitofusin-2 (Mfn-2) is a dynamin-like protein that is involved in the rearrangement of the outer mitochondrial membrane. Research using various experimental systems has shown that Mfn-2 is a mediator of mitochondrial fusion, an evolutionarily conserved process responsible for the surveillance of mitochondrial homeostasis. Here, we find that cardiac myocyte mitochondria lacking Mfn-2 are pleiomorphic and have the propensity to become enlarged. Consistent with an underlying mild mitochondrial dysfunction, Mfn-2-deficient mice display modest cardiac hypertrophy accompanied by slight functional deterioration. The absence of Mfn-2 is associated with a marked delay in mitochondrial permeability transition downstream of Ca(2+) stimulation or due to local generation of reactive oxygen species (ROSMolecular and cellular biologyMitofusin-2 maintains mitochondrial structure and contributes to stress-induced permeability transition in cardiac myocytes.PMC3067905HL064750HL102874R21 HL102874N01HV28178AG34972R01 HL061639P01 HL074237AG15052R01 AG034972R37 AG015052P01 HL068758HL68758R01 AG015052HL061639R01 HL064750HL074237Luptak IRiley DDColucci WSStanley WCWalsh KLederer WJPapanicolaou KNO'Shea KMNgoh GAKhairallah RJChikando ALugus JJfalseMitofusin-2 maintains mitochondrial structure and contributes to stress-induced permeability transition in cardiac myocytes.Mitofusin-2 (Mfn-2) is a dynamin-like protein that is involved in the rearrangement of the outer mitochondrial membrane. Research using various experimental systems has shown that Mfn-2 is a mediator of mitochondrial fusion, an evolutionarily conserved process responsible for the surveillance of mitochondrial homeostasis. Here, we find that cardiac myocyte mitochondria lacking Mfn-2 are pleiomorphic and have the propensity to become enlarged. Consistent with an underlying mild mitochondrial dysfunction, Mfn-2-deficient mice display modest cardiac hypertrophy accompanied by slight functional deterioration. The absence of Mfn-2 is associated with a marked delay in mitochondrial permeability transition downstream of Ca(2+) stimulation or due to local generation of reactive oxygen species (ROS2011-01-01T00:00:00Z2011 Mar2025-04-21T21:16:38.418Z2019-03-27T00:40:15ZS-EPMC30679052124537310.1128/mcb.00911-1010.1128/MCB.00911-10