{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Kim H"],"funding":["U.S. Department of Health & Human Services | NIH | National Institute of Arthritis and Musculoskeletal and Skin Diseases (NIAMS)","National Research Foundation of Korea (NRF)","U.S. Department of Health & Human Services | NIH | National Institute of Arthritis and Musculoskeletal and Skin Diseases","NCI NIH HHS","National Research Foundation of Korea","NIAMS NIH HHS"],"pagination":["48"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC11350122"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["12(1)"],"pubmed_abstract":["Osteoclasts are multinucleated bone-resorbing cells, and their formation is tightly regulated to prevent excessive bone loss. However, the mechanisms by which osteoclast formation is restricted remain incompletely determined. Here, we found that sterol regulatory element binding protein 2 (SREBP2) functions as a negative regulator of osteoclast formation and inflammatory bone loss. Cholesterols and SREBP2, a key transcription factor for cholesterol biosynthesis, increased in the late phase of osteoclastogenesis. The ablation of SREBP2 in myeloid cells resulted in increased in vivo and in vitro osteoclastogenesis, leading to low bone mass. Moreover, deletion of SREBP2 accelerated inflammatory bone destruction in murine inflammatory osteolysis and arthritis models. SREBP2-mediated regulation"],"journal":["Bone research"],"pubmed_title":["SREBP2 restricts osteoclast differentiation and activity by regulating IRF7 and limits inflammatory bone erosion."],"pmcid":["PMC11350122"],"funding_grant_id":["AR068118","R01 AR069562","R01 AR073156","2020R1A6A3A03037133","AR073156","P30 CA008748","AR069562","R03 AR068118"],"pubmed_authors":["Pannellini T","Park-Min KH","Kim H","Giannopoulou E","Bae S","Kaneko K","Mizuno M","Umemoto A","Deng L","Choi IA"],"additional_accession":[]},"is_claimable":false,"name":"SREBP2 restricts osteoclast differentiation and activity by regulating IRF7 and limits inflammatory bone erosion.","description":"Osteoclasts are multinucleated bone-resorbing cells, and their formation is tightly regulated to prevent excessive bone loss. However, the mechanisms by which osteoclast formation is restricted remain incompletely determined. Here, we found that sterol regulatory element binding protein 2 (SREBP2) functions as a negative regulator of osteoclast formation and inflammatory bone loss. Cholesterols and SREBP2, a key transcription factor for cholesterol biosynthesis, increased in the late phase of osteoclastogenesis. The ablation of SREBP2 in myeloid cells resulted in increased in vivo and in vitro osteoclastogenesis, leading to low bone mass. Moreover, deletion of SREBP2 accelerated inflammatory bone destruction in murine inflammatory osteolysis and arthritis models. SREBP2-mediated regulation","dates":{"release":"2024-01-01T00:00:00Z","publication":"2024 Aug","modification":"2026-04-07T14:53:11.367Z","creation":"2025-04-07T12:31:31.424Z"},"accession":"S-EPMC11350122","cross_references":{"pubmed":["39191742"],"doi":["10.1038/s41413-024-00354-4"]}}