Mitochondrial Fission Process 1 controls inner membrane integrity and protects against heart failure.
Journal
Nature communications
ISSN: 2041-1723
Titre abrégé: Nat Commun
Pays: England
ID NLM: 101528555
Informations de publication
Date de publication:
04 11 2022
04 11 2022
Historique:
received:
22
12
2021
accepted:
21
10
2022
pubmed:
6
11
2022
medline:
9
11
2022
entrez:
5
11
2022
Statut:
epublish
Résumé
Mitochondria are paramount to the metabolism and survival of cardiomyocytes. Here we show that Mitochondrial Fission Process 1 (MTFP1) is an inner mitochondrial membrane (IMM) protein that is dispensable for mitochondrial division yet essential for cardiac structure and function. Constitutive knockout of cardiomyocyte MTFP1 in mice resulted in a fatal, adult-onset dilated cardiomyopathy accompanied by extensive mitochondrial and cardiac remodeling during the transition to heart failure. Prior to the onset of disease, knockout cardiac mitochondria displayed specific IMM defects: futile proton leak dependent upon the adenine nucleotide translocase and an increased sensitivity to the opening of the mitochondrial permeability transition pore, with which MTFP1 physically and genetically interacts. Collectively, our data reveal new functions of MTFP1 in the control of bioenergetic efficiency and cell death sensitivity and define its importance in preventing pathogenic cardiac remodeling.
Identifiants
pubmed: 36333300
doi: 10.1038/s41467-022-34316-3
pii: 10.1038/s41467-022-34316-3
pmc: PMC9636241
doi:
Substances chimiques
Membrane Proteins
0
Mitochondrial Membrane Transport Proteins
0
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
6634Informations de copyright
© 2022. The Author(s).
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