{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Lin C"],"funding":["U.S. Department of Health & Human Services | NIH | National Institute of Arthritis and Musculoskeletal and Skin Diseases","Pershing Square Foundation"],"pagination":["6869"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC9652319"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["13(1)"],"pubmed_abstract":["Although skeletal progenitors provide a reservoir for bone-forming osteoblasts, the major energy source for their osteogenesis remains unclear. Here, we demonstrate a requirement for mitochondrial oxidative phosphorylation in the osteogenic commitment and differentiation of skeletal progenitors. Deletion of Evolutionarily Conserved Signaling Intermediate in Toll pathways (ECSIT) in skeletal progenitors hinders bone formation and regeneration, resulting in skeletal deformity, defects in the bone marrow niche and spontaneous fractures followed by persistent nonunion. Upon skeletal fracture, Ecsit-deficient skeletal progenitors migrate to adjacent skeletal muscle causing muscle atrophy. These phenotypes are intrinsic to ECSIT function in skeletal progenitors, as little skeletal abnormalities "],"journal":["Nature communications"],"pubmed_title":["Impaired mitochondrial oxidative metabolism in skeletal progenitor cells leads to musculoskeletal disintegration."],"pmcid":["PMC9652319"],"funding_grant_id":["R01AR075585"],"pubmed_authors":["Greenblatt MB","Chaugule S","Emerson CP","Qiu Q","Gao G","Li R","Oh WT","DeSouza N","Ghosh S","Shim JH","Lin C","Zhu LJ","Li S","Chen Z","John AA","Haynes C","Xie J","Yang YS","Guo D","Yang Q"],"additional_accession":[]},"is_claimable":false,"name":"Impaired mitochondrial oxidative metabolism in skeletal progenitor cells leads to musculoskeletal disintegration.","description":"Although skeletal progenitors provide a reservoir for bone-forming osteoblasts, the major energy source for their osteogenesis remains unclear. Here, we demonstrate a requirement for mitochondrial oxidative phosphorylation in the osteogenic commitment and differentiation of skeletal progenitors. Deletion of Evolutionarily Conserved Signaling Intermediate in Toll pathways (ECSIT) in skeletal progenitors hinders bone formation and regeneration, resulting in skeletal deformity, defects in the bone marrow niche and spontaneous fractures followed by persistent nonunion. Upon skeletal fracture, Ecsit-deficient skeletal progenitors migrate to adjacent skeletal muscle causing muscle atrophy. These phenotypes are intrinsic to ECSIT function in skeletal progenitors, as little skeletal abnormalities ","dates":{"release":"2022-01-01T00:00:00Z","publication":"2022 Nov","modification":"2026-06-01T02:12:53.678Z","creation":"2025-02-19T01:28:35.397Z"},"accession":"S-EPMC9652319","cross_references":{"pubmed":["36369293"],"doi":["10.1038/s41467-022-34694-8"]}}