{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Papanicolaou KN"],"funding":["NIA NIH HHS","NHLBI NIH HHS"],"pagination":["1309-28"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC3067905"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["31(6)"],"pubmed_abstract":["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 (ROS"],"journal":["Molecular and cellular biology"],"pubmed_title":["Mitofusin-2 maintains mitochondrial structure and contributes to stress-induced permeability transition in cardiac myocytes."],"pmcid":["PMC3067905"],"funding_grant_id":["HL064750","HL102874","R21 HL102874","N01HV28178","AG34972","R01 HL061639","P01 HL074237","AG15052","R01 AG034972","R37 AG015052","P01 HL068758","HL68758","R01 AG015052","HL061639","R01 HL064750","HL074237"],"pubmed_authors":["Luptak I","Riley DD","Colucci WS","Stanley WC","Walsh K","Lederer WJ","Papanicolaou KN","O'Shea KM","Ngoh GA","Khairallah RJ","Chikando A","Lugus JJ"],"additional_accession":[]},"is_claimable":false,"name":"Mitofusin-2 maintains mitochondrial structure and contributes to stress-induced permeability transition in cardiac myocytes.","description":"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 (ROS","dates":{"release":"2011-01-01T00:00:00Z","publication":"2011 Mar","modification":"2025-04-21T21:16:38.418Z","creation":"2019-03-27T00:40:15Z"},"accession":"S-EPMC3067905","cross_references":{"pubmed":["21245373"],"doi":["10.1128/mcb.00911-10","10.1128/MCB.00911-10"]}}