NAD depletion in skeletal muscle does not compromise muscle function or accelerate aging

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dc.contributor.authorChubanava, Sabina
dc.contributor.authorKaravaeva, Iuliia
dc.contributor.authorEhrlich, Amy M.
dc.contributor.authorJusticia, Roger M.
dc.contributor.authorBasse, Astrid L.
dc.contributor.authorKulik, Ivan
dc.contributor.authorDalbram, Emilie
dc.contributor.authorAhwazi, Danial
dc.contributor.authorHeaselgrave, Samuel R.
dc.contributor.authorTrost, Kajetan
dc.contributor.authorStocks, Ben
dc.contributor.authorHodek, Ondrej
dc.contributor.authorRodrigues, Raissa N.
dc.contributor.authorHavelund, Jesper F.
dc.contributor.authorSchlabs, Farina L.
dc.contributor.authorLarsen, Steen
dc.contributor.authorYonamine, Caio Y.
dc.contributor.authorHenríquez-Olguín, Carlos
dc.contributor.authorGiustarini, Daniela
dc.contributor.authorRossi, Ranieri
dc.contributor.authorGerhart-Hines, Zachary
dc.contributor.authorMoritz, Thomas
dc.contributor.authorZierath, Juleen R.
dc.contributor.authorSakamoto, Kei
dc.contributor.authorJensen, Thomas E.
dc.contributor.authorFærgeman, Nils J.
dc.contributor.authorLavery, Gareth G.
dc.contributor.authorDeshmukh, Atul S.
dc.contributor.authorTreebak, Jonas T.
dc.date.accessioned2025-10-28T18:49:34Z
dc.date.available2025-10-28T18:49:34Z
dc.date.issued0022-06-25
dc.description.abstractNicotinamide adenine dinucleotide (NAD) is a ubiquitous electron carrier essential for energy metabolism and post-translational modification of numerous regulatory proteins. Dysregulations of NAD metabolism are widely regarded as detrimental to health, with NAD depletion commonly implicated in aging. However, the extent to which cellular NAD concentration can decline without adverse consequences remains unclear. To investigate this, we generated a mouse model in which nicotinamide phosphoribosyltransferase (NAMPT)-mediated NAD+ biosynthesis was disrupted in adult skeletal muscle. The intervention resulted in an 85% reduction in muscle NAD+ abundance while maintaining tissue integrity and functionality, as demonstrated by preserved muscle morphology, contractility, and exercise tolerance. This absence of functional impairments was further supported by intact mitochondrial respiratory capacity and unaltered muscle transcriptomic and proteomic profiles. Furthermore, lifelong NAD depletion did not accelerate muscle aging or impair whole-body metabolism. Collectively, these findings suggest that NAD depletion does not contribute to age-related decline in skeletal muscle function.
dc.identifier.citationCell Metabolism, Vol. 37, N° 7 (2025) p.1460 - 1481.
dc.identifier.doihttps://doi.org/10.1016/j.cmet.2025.04.002
dc.identifier.issn1550-4131
dc.identifier.issne1932-7420
dc.identifier.orcidhttps://orcid.org/0000-0002-9315-9365
dc.identifier.urihttps://hdl.handle.net/20.500.12254/4363
dc.language.isoen
dc.publisherElsevier
dc.rightsAtribución-NoComercial-CompartirIgual 3.0 Chile (CC BY-NC-SA 3.0 CL)
dc.rights.urihttp://creativecommons.org/licenses/by-nc-sa/3.0/cl/
dc.subjectNAD metabolism
dc.subjectSkeletal muscle
dc.subjectMitochondrial
dc.subjectSupercomplexes
dc.titleNAD depletion in skeletal muscle does not compromise muscle function or accelerate aging
dc.typeArticle
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