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However, the co-occurrence of osteoporosis and sarcopenia remains unclear. We performed single-cell 5\u2032 RNA-seq on human skeletal muscle tissues and investigated the enrichment of heritability for musculoskeletal traits in cell type specific cis-regulatory regions. We found the fibroblast-specific cis-regulatory regions are highly enriched in the heritability of bone mineral density (BMD). Using genome-wide association study, we identified estrogen receptor \u03b1 (ESR1) as a common transcription factor that correlated with both BMD and lean mass. We hypothesized that deficiency of estrogen signaling in fibroblast may attenuate musculoskeletal homeostasis. Therefore, we generated mice lacking Esr1 in PDGFR\u03b1 (a fibroblast marker)\u2009+\u2009cells (Esr1\u0394P\u03b1). Although muscle mass and grip strength were not different between groups, distal femoral BMD and cortical thickness were significantly lower in Esr1\u0394P\u03b1 compared to control. Bone histomorphometry showed that cortical bone in Esr1\u0394P\u03b1 exhibited a high turnover bone phenotype. Bulk RNA-seq using PDGFR\u03b1+ cells revealed that insulin-like growth factor-binding protein 5 (Igfbp5) expression was significantly higher in Esr1\u0394P\u03b1 compared to control. Furthermore, serum IGFBP5 level was significantly higher in Esr1\u0394P\u03b1. IGFBP5 treatment in vitro significantly suppressed osteoblast differentiation and facilitated osteoclast differentiation. These results suggest that estrogen signaling in PDGFR\u03b1+ cells suppresses Igfbp5 expression, then maintains bone mass, indicating that estrogen signaling in PDGFR\u03b1+ cells plays a significant role in bone metabolism.<\/jats:p>","DOI":"10.1093\/jbmrpl\/ziaf178","type":"journal-article","created":{"date-parts":[[2025,11,6]],"date-time":"2025-11-06T13:22:58Z","timestamp":1762435378000},"source":"Crossref","is-referenced-by-count":0,"title":["Estrogen signaling in PDGFR\u03b1+ cells positively regulates cortical bone metabolism via IGFBP5 in female mice"],"prefix":"10.1093","volume":"10","author":[{"given":"Aoi","family":"Ikedo","sequence":"first","affiliation":[{"name":"Division of Integrative Pathophysiology, Proteo-Science Center, PIAS, Ehime University , Toon 791-0295 ,","place":["Japan"]}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Reina","family":"Aoki","sequence":"additional","affiliation":[{"name":"Department of Hepato-Biliary-Pancreatic Surgery and 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