{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Kan C"],"funding":["Natural Science Foundation of Anhui Province (Anhui Provincial Natural Science Foundation)","Natural Science Foundation of Anhui Province","National Natural Science Foundation of China","National Key Research and Development Program of China","National Natural Science Foundation of China (National Science Foundation of China)"],"pagination":["62"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC9605967"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["10(1)"],"pubmed_abstract":["Heterotopic ossification (HO) is the abnormal formation of bone in extraskeletal sites. However, the mechanisms linking HO pathogenesis with bone mass dysfunction remain unclear. Here, we showed that mice harboring injury-induced and BMP4-dependent HO exhibit bone mass loss similar to that presented by patients with HO. Moreover, we found that injury-induced hyperinflammatory responses at the injury site triggered HO initiation but did not result in bone mass loss at 1 day post-injury (dpi). In contrast, a suppressive immune response promoted HO propagation and bone mass loss by 7 dpi. Correcting immune dysregulation by PD1/PDL1 blockade dramatically alleviated HO propagation and bone mass loss. We further demonstrated that fetuin-A (FetA), which has been frequently detected in HO lesions "],"journal":["Bone research"],"pubmed_title":["Fetuin-A is an immunomodulator and a potential therapeutic option in BMP4-dependent heterotopic ossification and associated bone mass loss."],"pmcid":["PMC9605967"],"funding_grant_id":["1508085MC45","1908085QH359","81870085","82102573","32070916","81670097"],"pubmed_authors":["Li G","Yang J","Liu J","Ni F","Dai Y","Meng X","Fan H","Zheng H","Kan C","Zhang Y","Wang S","Wang W","Fang S","Wei H","Wang X","Zhu W","Chen R","Zhou J"],"additional_accession":[]},"is_claimable":false,"name":"Fetuin-A is an immunomodulator and a potential therapeutic option in BMP4-dependent heterotopic ossification and associated bone mass loss.","description":"Heterotopic ossification (HO) is the abnormal formation of bone in extraskeletal sites. However, the mechanisms linking HO pathogenesis with bone mass dysfunction remain unclear. Here, we showed that mice harboring injury-induced and BMP4-dependent HO exhibit bone mass loss similar to that presented by patients with HO. Moreover, we found that injury-induced hyperinflammatory responses at the injury site triggered HO initiation but did not result in bone mass loss at 1 day post-injury (dpi). In contrast, a suppressive immune response promoted HO propagation and bone mass loss by 7 dpi. Correcting immune dysregulation by PD1/PDL1 blockade dramatically alleviated HO propagation and bone mass loss. We further demonstrated that fetuin-A (FetA), which has been frequently detected in HO lesions ","dates":{"release":"2022-01-01T00:00:00Z","publication":"2022 Oct","modification":"2025-04-21T23:35:59.916Z","creation":"2025-04-05T19:11:35.557Z"},"accession":"S-EPMC9605967","cross_references":{"pubmed":["36289197"],"doi":["10.1038/s41413-022-00232-x"]}}