{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Zhang Y"],"funding":["NICHD NIH HHS","NHLBI NIH HHS","NCI NIH HHS","NIAMS NIH HHS"],"pagination":["114587"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC11472345"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["43(8)"],"pubmed_abstract":["Cancer cachexia is a prevalent and often fatal wasting condition that cannot be fully reversed with nutritional interventions. Muscle atrophy is a central component of the syndrome, but the mechanisms whereby cancer leads to skeletal muscle atrophy are not well understood. We performed single-nucleus multi-omics on skeletal muscles from a mouse model of cancer cachexia and profiled the molecular changes in cachexic muscle. Our results revealed the activation of a denervation-dependent gene program that upregulates the transcription factor myogenin. Further studies showed that a myogenin-myostatin pathway promotes muscle atrophy in response to cancer cachexia. Short hairpin RNA inhibition of myogenin or inhibition of myostatin through overexpression of its endogenous inhibitor follistatin p"],"journal":["Cell reports"],"pubmed_title":["A molecular pathway for cancer cachexia-induced muscle atrophy revealed at single-nucleus resolution."],"pmcid":["PMC11472345"],"funding_grant_id":["R01 AR067294","P50 HD087351","R01 AR071980","P30 CA008748","R01 HL130253","U54 HD087351","P30 CA142543","R01 AR080676"],"pubmed_authors":["Xu L","Polanco PM","Brekken RA","Chen K","Liu N","Huang H","Bassel-Duby R","Dos Santos M","Cai C","Zhang Y","Cano Hernandez K","Iyengar P","Infante R","Olson EN","Caijgas A"],"additional_accession":[]},"is_claimable":false,"name":"A molecular pathway for cancer cachexia-induced muscle atrophy revealed at single-nucleus resolution.","description":"Cancer cachexia is a prevalent and often fatal wasting condition that cannot be fully reversed with nutritional interventions. Muscle atrophy is a central component of the syndrome, but the mechanisms whereby cancer leads to skeletal muscle atrophy are not well understood. We performed single-nucleus multi-omics on skeletal muscles from a mouse model of cancer cachexia and profiled the molecular changes in cachexic muscle. Our results revealed the activation of a denervation-dependent gene program that upregulates the transcription factor myogenin. Further studies showed that a myogenin-myostatin pathway promotes muscle atrophy in response to cancer cachexia. Short hairpin RNA inhibition of myogenin or inhibition of myostatin through overexpression of its endogenous inhibitor follistatin p","dates":{"release":"2024-01-01T00:00:00Z","publication":"2024 Aug","modification":"2025-04-04T01:25:36.009Z","creation":"2025-04-04T01:25:36.009Z"},"accession":"S-EPMC11472345","cross_references":{"pubmed":["39116208"],"doi":["10.1016/j.celrep.2024.114587"]}}