{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,4,7]],"date-time":"2026-04-07T22:13:20Z","timestamp":1775600000747,"version":"3.50.1"},"reference-count":45,"publisher":"American Physiological Society","issue":"10","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Cell Physiology"],"published-print":{"date-parts":[[2016,5,15]]},"abstract":"<jats:p> The bone-resorbing osteoclast (OC) is essential for bone homeostasis, yet deregulation of OCs contributes to diseases such as osteoporosis, osteopetrosis, and rheumatoid arthritis. Here we show that histone deacetylase 2 (HDAC2) is a key positive regulator during receptor activator of nuclear factor-\u03baB ligand (RANKL)-induced osteoclastogenesis and bone resorption. Bone marrow macrophages (BMMs) showed increased HDAC2 expression during osteoclastogenesis. HDAC2 overexpression enhanced, whereas HDAC2 deletion suppressed osteoclastogenesis and bone resorption using lentivirus infection. Mechanistically, upon RANKL activation, HDAC2 activated Akt; Akt directly phosphorylates and abrogates Forkhead box protein O1 (FoxO1), which is a negative regulator during osteoclastogenesis through reducing reactive oxygen species. HDAC2 deletion in BMMs resulted in decreased Akt activation and increased FoxO1 activity during osteoclastogenesis. In conclusion, HDAC2 activates Akt thus suppresses FoxO1 transcription results in enhanced osteoclastogenesis. Our data imply the potential value of HDAC2 as a new target in regulating osteoclast differentiation and function. <\/jats:p>","DOI":"10.1152\/ajpcell.00351.2015","type":"journal-article","created":{"date-parts":[[2016,3,10]],"date-time":"2016-03-10T04:23:27Z","timestamp":1457583807000},"page":"C780-C787","source":"Crossref","is-referenced-by-count":33,"title":["HDAC2 regulates FoxO1 during RANKL-induced osteoclastogenesis"],"prefix":"10.1152","volume":"310","author":[{"given":"Ce","family":"Dou","sequence":"first","affiliation":[{"name":"Department of Biomedical Materials Science, School of Biomedical Engineering, Third Military Medical University, Chongqing, China; and"},{"name":"Department of Orthopedics, Southwest Hospital, Third Military Medical University, Chongqing, China"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Nan","family":"Li","sequence":"additional","affiliation":[{"name":"Department of Biomedical Materials Science, School of Biomedical Engineering, Third Military Medical University, Chongqing, China; 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