<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Arc-Chagnaud C</submitter><funding>Instituto de Salud Carlos III</funding><funding>Ministerio de Ciencia e Innovación</funding><funding>Montana Department of Agriculture</funding><funding>Advanced Foods and Materials Canada</funding><funding>Fundació la Marató de TV3</funding><funding>Fundación General CSIC</funding><funding>Generalitat Valenciana</funding><funding>European Regional Development Fund</funding><pagination>1879-1896</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC8718080</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>12(6)</volume><pubmed_abstract>&lt;h4>Background&lt;/h4>Frailty is a major age-associated syndrome leading to disability. Oxidative damage plays a significant role in the promotion of frailty. The cellular antioxidant system relies on reduced nicotinamide adenine dinucleotide phosphate (NADPH) that is highly dependent on glucose 6-P dehydrogenase (G6PD). The G6PD-overexpressing mouse (G6PD-Tg) is protected against metabolic stresses. Our aim was to examine whether this protection delays frailty.&lt;h4>Methods&lt;/h4>Old wild-type (WT) and G6PD-Tg mice were evaluated longitudinally in terms of frailty. Indirect calorimetry, transcriptomic profile, and different skeletal muscle quality markers and muscle regenerative capacity were also investigated.&lt;h4>Results&lt;/h4>The percentage of frail mice was significantly lower in the G6PD-Tg th</pubmed_abstract><journal>Journal of cachexia, sarcopenia and muscle</journal><pubmed_title>Glucose 6-P dehydrogenase delays the onset of frailty by protecting against muscle damage.</pubmed_title><pmcid>PMC8718080</pmcid><funding_grant_id>202033</funding_grant_id><funding_grant_id>CB16/10/00435</funding_grant_id><pubmed_authors>Arc-Chagnaud C</pubmed_authors><pubmed_authors>Serna E</pubmed_authors><pubmed_authors>Gomez-Cabrera MC</pubmed_authors><pubmed_authors>Garcia-Dominguez E</pubmed_authors><pubmed_authors>Vina J</pubmed_authors><pubmed_authors>Correas AG</pubmed_authors><pubmed_authors>Chopard A</pubmed_authors><pubmed_authors>Munoz-Canoves P</pubmed_authors><pubmed_authors>Sebastia V</pubmed_authors><pubmed_authors>Salvador-Pascual A</pubmed_authors><pubmed_authors>Fernandez-Marcos PJ</pubmed_authors><pubmed_authors>Olaso-Gonzalez G</pubmed_authors><pubmed_authors>Brioche T</pubmed_authors><pubmed_authors>Serrano AL</pubmed_authors><pubmed_authors>Serrano M</pubmed_authors></additional><is_claimable>false</is_claimable><name>Glucose 6-P dehydrogenase delays the onset of frailty by protecting against muscle damage.</name><description>&lt;h4>Background&lt;/h4>Frailty is a major age-associated syndrome leading to disability. Oxidative damage plays a significant role in the promotion of frailty. The cellular antioxidant system relies on reduced nicotinamide adenine dinucleotide phosphate (NADPH) that is highly dependent on glucose 6-P dehydrogenase (G6PD). The G6PD-overexpressing mouse (G6PD-Tg) is protected against metabolic stresses. Our aim was to examine whether this protection delays frailty.&lt;h4>Methods&lt;/h4>Old wild-type (WT) and G6PD-Tg mice were evaluated longitudinally in terms of frailty. Indirect calorimetry, transcriptomic profile, and different skeletal muscle quality markers and muscle regenerative capacity were also investigated.&lt;h4>Results&lt;/h4>The percentage of frail mice was significantly lower in the G6PD-Tg th</description><dates><release>2021-01-01T00:00:00Z</release><publication>2021 Dec</publication><modification>2026-05-09T11:56:46.743Z</modification><creation>2022-02-11T15:04:08.992Z</creation></dates><accession>S-EPMC8718080</accession><cross_references><pubmed>34704386</pubmed><doi>10.1002/jcsm.12792</doi></cross_references></HashMap>