{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,3]],"date-time":"2026-08-03T23:46:16Z","timestamp":1785800776765,"version":"3.56.0"},"reference-count":112,"publisher":"American Society for Clinical Investigation","issue":"22","funder":[{"name":"NIH","award":["R01 AR066735"],"award-info":[{"award-number":["R01 AR066735"]}]},{"name":"NIH","award":["AR070155"],"award-info":[{"award-number":["AR070155"]}]},{"name":"Doris Duke Charitable Foundation Clinical Scientist Development Award","award":["2014099"],"award-info":[{"award-number":["2014099"]}]},{"DOI":"10.13039\/100000912","name":"March of Dimes","doi-asserted-by":"crossref","award":["1-FY14-211"],"award-info":[{"award-number":["1-FY14-211"]}],"id":[{"id":"10.13039\/100000912","id-type":"DOI","asserted-by":"crossref"}]},{"name":"University of California  Department of Medicine","award":["University of California  Department of Medicine"],"award-info":[{"award-number":["University of California  Department of Medicine"]}]},{"name":"Radiant Hope Foundation","award":["Radiant Hope Foundation"],"award-info":[{"award-number":["Radiant Hope Foundation"]}]},{"name":"California Institute for Regenerative Medicine Fellowship Program to UCSF","award":["TG2-01153"],"award-info":[{"award-number":["TG2-01153"]}]},{"name":"NIH","award":["T32DK007161"],"award-info":[{"award-number":["T32DK007161"]}]},{"name":"NIH","award":["F32HD091025"],"award-info":[{"award-number":["F32HD091025"]}]},{"name":"Alpha-Omega-Alpha Summer Research Fellowship","award":["Alpha-Omega-Alpha Summer Research Fellowship"],"award-info":[{"award-number":["Alpha-Omega-Alpha Summer Research Fellowship"]}]},{"DOI":"10.13039\/100008069","name":"UCSF","doi-asserted-by":"crossref","award":["Russell\/Engleman Arthritis Center at UCSF"],"award-info":[{"award-number":["Russell\/Engleman Arthritis Center at UCSF"]}],"id":[{"id":"10.13039\/100008069","id-type":"DOI","asserted-by":"crossref"}]},{"name":"the Department of Veteran\u2019s Affairs Health Care System","award":["the Department of Veteran\u2019s Affairs Health Care System"],"award-info":[{"award-number":["the Department of Veteran\u2019s Affairs Health Care System"]}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2018,11,15]]},"abstract":"<jats:p>\n                    <jats:bold>BACKGROUND.<\/jats:bold>\n                    Inflammation helps regulate normal growth and tissue repair. Although bone morphogenetic proteins (BMPs) and inflammation are known contributors to abnormal bone formation, how these pathways interact in ossification remains unclear.\n                  <\/jats:p>\n                  <jats:p>\n                    <jats:bold>METHODS.<\/jats:bold>\n                    We examined this potential link in patients with fibrodysplasia ossificans progressiva (FOP), a genetic condition of progressive heterotopic ossification caused by activating mutations in the Activin A type I receptor (ACVR1\/ALK2). FOP patients show exquisite sensitivity to trauma, suggesting that BMP pathway activation may alter immune responses. We studied primary blood, monocyte, and macrophage samples from control and FOP subjects using multiplex cytokine, gene expression, and protein analyses; examined CD14\n                    <jats:sup>\n                      <jats:sup>+<\/jats:sup>\n                    <\/jats:sup>\n                    primary monocyte and macrophage responses to TLR ligands; and assayed BMP, TGF-\u03b2 activated kinase 1 (TAK1), and NF-\n                    <jats:bold>\u03ba<\/jats:bold>\n                    B pathways.\n                  <\/jats:p>\n                  <jats:p>\n                    <jats:bold>RESULTS.<\/jats:bold>\n                    FOP subjects at baseline without clinically evident heterotopic ossification showed increased serum IL-3, IL-7, IL-8, and IL-10. CD14\n                    <jats:sup>\n                      <jats:sup>+<\/jats:sup>\n                    <\/jats:sup>\n                    primary monocytes treated with the TLR4 activator LPS showed increased CCL5, CCR7, and CXCL10; abnormal cytokine\/chemokine secretion; and prolonged activation of the NF-\n                    <jats:bold>\u03ba<\/jats:bold>\n                    B pathway. FOP macrophages derived from primary monocytes also showed abnormal cytokine\/chemokine secretion, increased TGF-\u03b2 production, and p38MAPK activation. Surprisingly, SMAD phosphorylation was not significantly changed in the FOP monocytes\/macrophages.\n                  <\/jats:p>\n                  <jats:p>\n                    <jats:bold>CONCLUSIONS.<\/jats:bold>\n                    Abnormal ACVR1 activity causes a proinflammatory state via increased NF-\n                    <jats:bold>\u03ba<\/jats:bold>\n                    B and p38MAPK activity. Similar changes may contribute to other types of heterotopic ossification, such as in scleroderma and dermatomyositis; after trauma; or with recombinant BMP-induced bone fusion. Our findings suggest that chronic antiinflammatory treatment may be useful for heterotopic ossification.\n                  <\/jats:p>","DOI":"10.1172\/jci.insight.122958","type":"journal-article","created":{"date-parts":[[2018,11,14]],"date-time":"2018-11-14T11:01:38Z","timestamp":1542193298000},"source":"Crossref","is-referenced-by-count":102,"title":["NF-\u03baB\/MAPK activation underlies ACVR1-mediated inflammation in human heterotopic ossification"],"prefix":"10.1172","volume":"3","author":[{"given":"Emilie","family":"Barruet","sequence":"first","affiliation":[{"name":"Division of Endocrinology and Metabolism, Department of Medicine, and the Institute for Human Genetics, UCSF, San Francisco, California, USA."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Blanca M.","family":"Morales","sequence":"additional","affiliation":[{"name":"Division of Endocrinology and Metabolism, Department of Medicine, and the Institute for Human Genetics, UCSF, San Francisco, 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