{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Gao Y"],"funding":["NIAID NIH HHS","NHLBI NIH HHS","American Heart Association Inc","National Institutes of Health","Leukemia Research Foundation","National Heart Lung and Blood Institute","University of Texas MD Anderson Cancer Center","Cancer Prevention and Research Institute of Texas","Cedars-Sinai Health System","Burroughs Wellcome Fund","National Cancer Institute","NCI NIH HHS","NIH HHS"],"pagination":["101969"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC11278897"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["86"],"pubmed_abstract":["Objectives
Cachexia is a metabolic disorder and comorbidity with cancer and heart failure. The syndrome impacts more than thirty million people worldwide, accounting for 20% of all cancer deaths. In acute myeloid leukemia, somatic mutations of the metabolic enzyme isocitrate dehydrogenase 1 and 2 cause the production of the oncometabolite D2-hydroxyglutarate (D2-HG). Increased production of D2-HG is associated with heart and skeletal muscle atrophy, but the mechanistic links between metabolic and proteomic remodeling remain poorly understood. Therefore, we assessed how oncometabolic stress by D2-HG activates autophagy and drives skeletal muscle loss.Methods
We quantified genomic, metabolomic, and proteomic changes in cultured skeletal muscle cells and mouse models of IDH-mu"],"journal":["Molecular metabolism"],"pubmed_title":["Autophagic signaling promotes systems-wide remodeling in skeletal muscle upon oncometabolic stress by D2-HG."],"pmcid":["PMC11278897"],"funding_grant_id":["S10 OD012304","17POST33660221","R00 HL141702","K01 AI148593","K01-AI148593","R00-HL-141702","S10OD012304-01","R01-HL132075","R01-HL-061483","15RDM005","P30 CA016672","RP130397","R01-HL144509","R01 HL132075","R01 HL144509","R01 HL061483","U01 CA235510","U01CA235510"],"pubmed_authors":["Tan L","Salazar RL","Spivia W","Vitrac H","Karlstaedt A","Dinh AQ","Lorenzi PL","Hanson BM","Raedschelders K","Taegtmeyer H","Kim K","McNavish D","Azinas S","Gould BD","Burks HB","Gottlieb RA","Gao Y","Taylor DJR","Soedkamp D","Van Eyk JE","Guzman AG","Schiffer W"],"additional_accession":[]},"is_claimable":false,"name":"Autophagic signaling promotes systems-wide remodeling in skeletal muscle upon oncometabolic stress by D2-HG.","description":"Objectives
Cachexia is a metabolic disorder and comorbidity with cancer and heart failure. The syndrome impacts more than thirty million people worldwide, accounting for 20% of all cancer deaths. In acute myeloid leukemia, somatic mutations of the metabolic enzyme isocitrate dehydrogenase 1 and 2 cause the production of the oncometabolite D2-hydroxyglutarate (D2-HG). Increased production of D2-HG is associated with heart and skeletal muscle atrophy, but the mechanistic links between metabolic and proteomic remodeling remain poorly understood. Therefore, we assessed how oncometabolic stress by D2-HG activates autophagy and drives skeletal muscle loss.Methods
We quantified genomic, metabolomic, and proteomic changes in cultured skeletal muscle cells and mouse models of IDH-mu","dates":{"release":"2024-01-01T00:00:00Z","publication":"2024 Aug","modification":"2026-06-01T09:02:17.989Z","creation":"2025-08-31T03:05:22.251Z"},"accession":"S-EPMC11278897","cross_references":{"pubmed":["38908793"],"doi":["10.1016/j.molmet.2024.101969"]}}