{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,6,8]],"date-time":"2026-06-08T10:05:47Z","timestamp":1780913147862,"version":"3.54.1"},"reference-count":26,"publisher":"Wiley","issue":"1","license":[{"start":{"date-parts":[[2026,6,8]],"date-time":"2026-06-08T00:00:00Z","timestamp":1780876800000},"content-version":"vor","delay-in-days":158,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"},{"start":{"date-parts":[[2026,1,1]],"date-time":"2026-01-01T00:00:00Z","timestamp":1767225600000},"content-version":"tdm","delay-in-days":0,"URL":"http:\/\/doi.wiley.com\/10.1002\/tdm_license_1.1"}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["International Journal of Endocrinology"],"published-print":{"date-parts":[[2026,1]]},"abstract":"<jats:sec>\n                    <jats:title>Objective<\/jats:title>\n                    <jats:p>This study elucidates the role of TRIM27 in osteogenic differentiation and osteoporosis pathogenesis, focusing on its regulatory mechanism through PPAR\u03b3.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>TRIM27 expression was assessed during osteogenic differentiation of bone marrow mesenchymal stem cells (BMSCs) via RT\u2010qPCR and western blot. TRIM27 was knocked down (sh\u2010TRIM27) or overexpressed (Lv\u2010TRIM27) to evaluate its impact on alkaline phosphatase (ALP) activity, mineralization (Alizarin Red S staining), and osteogenic markers (COL1A1, OPN, and OCN). An ovariectomized (OVX) mouse osteoporosis model was established to analyze TRIM27 expression and bone microstructure (H&amp;E staining). Co\u2010immunoprecipitation (Co\u2010IP) and cycloheximide chase assays identified TRIM27\u2013PPAR\u03b3 interactions and degradation dynamics. Rescue experiments combined sh\u2010TRIM27 with PPAR\u03b3 knockdown (sh\u2010PPAR\u03b3) or the agonist rosiglitazone (ROZ).<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      TRIM27 expression increased 2.1\u2010fold during BMSC osteogenic differentiation but decreased in OVX mice (\n                      <jats:italic>p<\/jats:italic>\n                      &lt; 0.01 vs. sham). TRIM27 overexpression enhanced ALP activity, mineralization, and osteogenic markers (\n                      <jats:italic>p<\/jats:italic>\n                      &lt; 0.05), while knockdown exerted opposite effects. TRIM27 directly bound PPAR\u03b3 and promoted its ubiquitin\u2010mediated degradation. PPAR\u03b3 knockdown reversed sh\u2010TRIM27\u2010mediated inhibition of osteogenesis. In OVX mice, Lv\u2010TRIM27 reduced bone loss by suppressing PPAR\u03b3, whereas ROZ abolished this protective effect.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusion<\/jats:title>\n                    <jats:p>TRIM27, as a key osteogenic promoter, ameliorates osteoporosis by targeting the degradation of PPAR\u03b3. Our research reveals the potential of TRIM27 in treating bone metabolism disorders and may become a potential target for the treatment of osteoporosis.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1155\/ije\/6777760","type":"journal-article","created":{"date-parts":[[2026,6,8]],"date-time":"2026-06-08T09:19:51Z","timestamp":1780910391000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["TRIM27 Ubiquitinates and Degrades PPAR\u03b3 to Promote Osteogenic Differentiation of BMSCs and Alleviate 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