<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Miller MJ</submitter><funding>National Institute of Arthritis and Musculoskeletal and Skin Diseases</funding><funding>NIA NIH HHS</funding><funding>NIAMS NIH HHS</funding><funding>National Institute on Aging</funding><pagination>e14097</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC11019130</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>23(4)</volume><pubmed_abstract>The loss of skeletal muscle mass during aging is a significant health concern linked to adverse outcomes in older individuals. Understanding the molecular basis of age-related muscle loss is crucial for developing strategies to combat this debilitating condition. Long noncoding RNAs (lncRNAs) are a largely uncharacterized class of biomolecules that have been implicated in cellular homeostasis and dysfunction across a many tissues and cell types. To identify lncRNAs that might contribute to skeletal muscle aging, we screened for lncRNAs whose expression was altered in vastus lateralis muscle from older compared to young adults. We identified FRAIL1 as an aging-induced lncRNA with high abundance in human skeletal muscle. In healthy young and older adults, skeletal muscle FRAIL1 was increased</pubmed_abstract><journal>Aging cell</journal><pubmed_title>Human myofiber-enriched aging-induced lncRNA FRAIL1 promotes loss of skeletal muscle function.</pubmed_title><pmcid>PMC11019130</pmcid><funding_grant_id>R01 AG054454</funding_grant_id><funding_grant_id>NIAMS R01 AR071762</funding_grant_id><funding_grant_id>NIA R44 AG047684</funding_grant_id><funding_grant_id>NIAMS R44 AR069400</funding_grant_id><funding_grant_id>R01 AG060637</funding_grant_id><funding_grant_id>R44 AG047684</funding_grant_id><funding_grant_id>NIA R01 AG054454</funding_grant_id><funding_grant_id>NIA R01 AG060637</funding_grant_id><funding_grant_id>R44 AR069400</funding_grant_id><pubmed_authors>Dasari S</pubmed_authors><pubmed_authors>Adams CM</pubmed_authors><pubmed_authors>Marcotte GR</pubmed_authors><pubmed_authors>Strub MD</pubmed_authors><pubmed_authors>Miller MJ</pubmed_authors><pubmed_authors>Kunz HE</pubmed_authors><pubmed_authors>Lanza IR</pubmed_authors><pubmed_authors>Arendt BK</pubmed_authors><pubmed_authors>Ebert SM</pubmed_authors><pubmed_authors>Gries KJ</pubmed_authors><pubmed_authors>Ryan Z</pubmed_authors></additional><is_claimable>false</is_claimable><name>Human myofiber-enriched aging-induced lncRNA FRAIL1 promotes loss of skeletal muscle function.</name><description>The loss of skeletal muscle mass during aging is a significant health concern linked to adverse outcomes in older individuals. Understanding the molecular basis of age-related muscle loss is crucial for developing strategies to combat this debilitating condition. Long noncoding RNAs (lncRNAs) are a largely uncharacterized class of biomolecules that have been implicated in cellular homeostasis and dysfunction across a many tissues and cell types. To identify lncRNAs that might contribute to skeletal muscle aging, we screened for lncRNAs whose expression was altered in vastus lateralis muscle from older compared to young adults. We identified FRAIL1 as an aging-induced lncRNA with high abundance in human skeletal muscle. In healthy young and older adults, skeletal muscle FRAIL1 was increased</description><dates><release>2024-01-01T00:00:00Z</release><publication>2024 Apr</publication><modification>2026-05-27T12:18:40.613Z</modification><creation>2025-04-06T00:48:01.265Z</creation></dates><accession>S-EPMC11019130</accession><cross_references><pubmed>38297807</pubmed><doi>10.1111/acel.14097</doi></cross_references></HashMap>