<HashMap><database>biostudies-literature</database><scores/><additional><omics_type>Unknown</omics_type><submitter>Mitchell W</submitter><funding>NIBIB NIH HHS</funding><funding>NIA NIH HHS</funding><funding>NIAMS NIH HHS</funding><pubmed_abstract>Aging-related decreases in cardiac and skeletal muscle function are strongly associated with various comorbidities. Elamipretide (ELAM), a novel mitochondrial-targeted peptide, has demonstrated broad therapeutic efficacy in ameliorating disease conditions associated with mitochondrial dysfunction across both clinical and pre-clinical models. ELAM is proposed to restore mitochondrial bioenergetic function by stabilizing inner membrane structure and increasing oxidative phosphorylation coupling and efficiency. Although ELAM treatment effectively attenuates physiological declines in multiple tissues in rodent aging models, it remains unclear whether these functional improvements correlate with favorable changes in molecular biomarkers of aging. Herein, we investigated the impact of 8-week ELA</pubmed_abstract><journal>bioRxiv : the preprint server for biology</journal><pagination>2024.10.30.620676</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC11565897</full_dataset_link><repository>biostudies-literature</repository><pubmed_title>The mitochondrial-targeted peptide therapeutic elamipretide improves cardiac and skeletal muscle function during aging without detectable changes in tissue epigenetic or transcriptomic age.</pubmed_title><pmcid>PMC11565897</pmcid><funding_grant_id>P01 AG047200</funding_grant_id><funding_grant_id>R01 AG078279</funding_grant_id><funding_grant_id>T32 AG066574</funding_grant_id><funding_grant_id>T32 EB016652</funding_grant_id><funding_grant_id>R56 AG078279</funding_grant_id><funding_grant_id>P01 AG001751</funding_grant_id><funding_grant_id>R01 AG065403</funding_grant_id><funding_grant_id>P30 AR074990</funding_grant_id><pubmed_authors>Pharaoh G</pubmed_authors><pubmed_authors>Gladyshev VN</pubmed_authors><pubmed_authors>Tyshkovskiy A</pubmed_authors><pubmed_authors>Marcinek DJ</pubmed_authors><pubmed_authors>Mitchell W</pubmed_authors><pubmed_authors>Campbell M</pubmed_authors></additional><is_claimable>false</is_claimable><name>The mitochondrial-targeted peptide therapeutic elamipretide improves cardiac and skeletal muscle function during aging without detectable changes in tissue epigenetic or transcriptomic age.</name><description>Aging-related decreases in cardiac and skeletal muscle function are strongly associated with various comorbidities. Elamipretide (ELAM), a novel mitochondrial-targeted peptide, has demonstrated broad therapeutic efficacy in ameliorating disease conditions associated with mitochondrial dysfunction across both clinical and pre-clinical models. ELAM is proposed to restore mitochondrial bioenergetic function by stabilizing inner membrane structure and increasing oxidative phosphorylation coupling and efficiency. Although ELAM treatment effectively attenuates physiological declines in multiple tissues in rodent aging models, it remains unclear whether these functional improvements correlate with favorable changes in molecular biomarkers of aging. Herein, we investigated the impact of 8-week ELA</description><dates><release>2024-01-01T00:00:00Z</release><publication>2024 Oct</publication><modification>2025-04-04T02:46:47.136Z</modification><creation>2025-04-04T02:46:47.136Z</creation></dates><accession>S-EPMC11565897</accession><cross_references><pubmed>39554099</pubmed><doi>10.1101/2024.10.30.620676</doi></cross_references></HashMap>