OxPhos defects cause hypermetabolism and reduce lifespan in cells and in patients with mitochondrial diseases

Autor: Gabriel Sturm, Kalpita R. Karan, Anna S. Monzel, Balaji Santhanam, Tanja Taivassalo, Céline Bris, Sarah A. Ware, Marissa Cross, Atif Towheed, Albert Higgins-Chen, Meagan J. McManus, Andres Cardenas, Jue Lin, Elissa S. Epel, Shamima Rahman, John Vissing, Bruno Grassi, Morgan Levine, Steve Horvath, Ronald G. Haller, Guy Lenaers, Douglas C. Wallace, Marie-Pierre St-Onge, Saeed Tavazoie, Vincent Procaccio, Brett A. Kaufman, Erin L. Seifert, Michio Hirano, Martin Picard
Jazyk: angličtina
Rok vydání: 2023
Předmět:
Zdroj: Communications Biology, Vol 6, Iss 1, Pp 1-22 (2023)
Druh dokumentu: article
ISSN: 2399-3642
DOI: 10.1038/s42003-022-04303-x
Popis: A meta-analysis of 17 cohorts of mitochondrial disease patients reveals that OxPhos defects are associated with signs of hypermetabolism. Experiments in patient-derived fibroblast show that mitochondrial OxPhos defects trigger hypermetabolism in a cell-autonomous manner and this is linked to accelerated telomere shortening and epigenetic aging.
Databáze: Directory of Open Access Journals
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