<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Huang TJ</submitter><funding>Natural Science Foundation of Jiangxi Province</funding><funding>Health Commission of Jiangxi Province</funding><pagination>142</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC11977089</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>82(1)</volume><pubmed_abstract>&lt;h4>Background&lt;/h4>Sarcopenia, the age-related decline in muscle mass and function, poses a major health risk to the elderly population. Although dietary advanced glycation end-products (AGEs) have been implicated in worsening sarcopenia, the precise molecular mechanisms remain unclear.&lt;h4>Methods&lt;/h4>A sarcopenia animal model was established by feeding a high AGE diet to C57BL/6 mice. Muscle function and mass were assessed using grip strength tests, and rotarod tests. Proteomic analysis was used to identify differentially expressed proteins. Immunoprecipitation, mass spectrometry, and co-immunoprecipitation were employed to investigate protein interactions both in vivo and in vitro. Quantitative reverse transcription PCR and Western blotting were conducted to measure gene and protein expr</pubmed_abstract><journal>Cellular and molecular life sciences : CMLS</journal><pubmed_title>Dietary advanced glycation end-products exacerbate sarcopenia onset by activating apoptosis through PRMT1-mediated CRTC3 arginine methylation.</pubmed_title><pmcid>PMC11977089</pmcid><funding_grant_id>20242BAB25539</funding_grant_id><funding_grant_id>202310009</funding_grant_id><pubmed_authors>Wan Q</pubmed_authors><pubmed_authors>Huang TJ</pubmed_authors><pubmed_authors>Li Q</pubmed_authors><pubmed_authors>Li YJ</pubmed_authors><pubmed_authors>Zheng JN</pubmed_authors><pubmed_authors>Shang S</pubmed_authors><pubmed_authors>Chen FX</pubmed_authors></additional><is_claimable>false</is_claimable><name>Dietary advanced glycation end-products exacerbate sarcopenia onset by activating apoptosis through PRMT1-mediated CRTC3 arginine methylation.</name><description>&lt;h4>Background&lt;/h4>Sarcopenia, the age-related decline in muscle mass and function, poses a major health risk to the elderly population. Although dietary advanced glycation end-products (AGEs) have been implicated in worsening sarcopenia, the precise molecular mechanisms remain unclear.&lt;h4>Methods&lt;/h4>A sarcopenia animal model was established by feeding a high AGE diet to C57BL/6 mice. Muscle function and mass were assessed using grip strength tests, and rotarod tests. Proteomic analysis was used to identify differentially expressed proteins. Immunoprecipitation, mass spectrometry, and co-immunoprecipitation were employed to investigate protein interactions both in vivo and in vitro. Quantitative reverse transcription PCR and Western blotting were conducted to measure gene and protein expr</description><dates><release>2025-01-01T00:00:00Z</release><publication>2025 Apr</publication><modification>2025-07-13T03:05:11.231Z</modification><creation>2025-07-13T03:05:11.231Z</creation></dates><accession>S-EPMC11977089</accession><cross_references><pubmed>40192801</pubmed><doi>10.1007/s00018-025-05657-1</doi></cross_references></HashMap>