{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,13]],"date-time":"2026-10-13T02:39:29Z","timestamp":1791859169518,"version":"4.3.4"},"reference-count":31,"publisher":"National Academy of Sciences","issue":"18","license":[{"start":{"date-parts":[[2026,4,28]],"date-time":"2026-04-28T00:00:00Z","timestamp":1777334400000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by-nc-nd\/4.0\/"}],"funder":[{"DOI":"10.13039\/100000062","name":"HHS | NIH | National Institute of Diabetes and Digestive and Kidney Diseases","doi-asserted-by":"publisher","award":["RO1 DK107670"],"award-info":[{"award-number":["RO1 DK107670"]}],"id":[{"id":"10.13039\/100000062","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000062","name":"HHS | NIH | National Institute of Diabetes and Digestive and Kidney Diseases","doi-asserted-by":"publisher","award":["RO1 DK107670"],"award-info":[{"award-number":["RO1 DK107670"]}],"id":[{"id":"10.13039\/100000062","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000062","name":"HHS | NIH | National Institute of Diabetes and Digestive and Kidney Diseases","doi-asserted-by":"publisher","award":["RO1 DK107670"],"award-info":[{"award-number":["RO1 DK107670"]}],"id":[{"id":"10.13039\/100000062","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000062","name":"HHS | NIH | National Institute of Diabetes and Digestive and Kidney Diseases","doi-asserted-by":"publisher","award":["DK095112"],"award-info":[{"award-number":["DK095112"]}],"id":[{"id":"10.13039\/100000062","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000062","name":"HHS | NIH | National Institute of Diabetes and Digestive and Kidney Diseases","doi-asserted-by":"publisher","award":["RO1 DK113627"],"award-info":[{"award-number":["RO1 DK113627"]}],"id":[{"id":"10.13039\/100000062","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000049","name":"HHS | NIH | National Institute on Aging","doi-asserted-by":"publisher","award":["U19 AG60917"],"award-info":[{"award-number":["U19 AG60917"]}],"id":[{"id":"10.13039\/100000049","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["www.pnas.org"],"crossmark-restriction":true},"short-container-title":["Proc. Natl. Acad. Sci. U.S.A."],"published-print":{"date-parts":[[2026,5,5]]},"abstract":"<jats:p>\n                    Erythroferrone (ERFE), secreted by erythroblasts, is regarded as a classical regulator of iron metabolism through its suppression of hepcidin. Thus, as a consequence of insufficient hepcidin suppression and reduced iron availability, global\n                    <jats:italic toggle=\"yes\">Erfe<\/jats:italic>\n                    <jats:sup>\u2013<\/jats:sup>\n                    <jats:italic toggle=\"yes\">\n                      <jats:sup>\/<\/jats:sup>\n                    <\/jats:italic>\n                    <jats:sup>\u2013<\/jats:sup>\n                    mice exhibit delayed recovery after phlebotomy. We have shown previously that, apart from erythroblasts, ERFE is notably expressed in osteoblasts. To explore the effect specifically of osteoblast-derived ERFE during stress erythropoiesis, we first created\n                    <jats:italic toggle=\"yes\">Erfe<\/jats:italic>\n                    <jats:sup>fl\/fl<\/jats:sup>\n                    mice, which were then crossed with\n                    <jats:italic toggle=\"yes\">Col2.3<\/jats:italic>\n                    -Cre mice to generate osteoblast-selective\n                    <jats:italic toggle=\"yes\">Erfe<\/jats:italic>\n                    mutants (or\n                    <jats:italic toggle=\"yes\">Col2.3<\/jats:italic>\n                    -Cre;\n                    <jats:italic toggle=\"yes\">Erfe<\/jats:italic>\n                    <jats:sup>fl\/fl<\/jats:sup>\n                    mice). The induction of stress erythropoiesis in these latter mice by phlebotomy resulted in reduced serum ERFE levels and increased liver\n                    <jats:italic toggle=\"yes\">Hamp<\/jats:italic>\n                    (hepcidin) expression. Importantly,\n                    <jats:italic toggle=\"yes\">Col2.3<\/jats:italic>\n                    -Cre;\n                    <jats:italic toggle=\"yes\">Erfe<\/jats:italic>\n                    <jats:sup>fl\/fl<\/jats:sup>\n                    mice showed a more robust red blood cell (RBC) recovery 6 d postphlebotomy, with no differences in bone marrow\n                    <jats:italic toggle=\"yes\">Erfe<\/jats:italic>\n                    relative to\n                    <jats:italic toggle=\"yes\">Erfe<\/jats:italic>\n                    <jats:sup>fl\/fl<\/jats:sup>\n                    mice. Furthermore, despite no differences in the baseline RBC count, reticulocyte count, spleen size, or bone marrow cellularity, osteoblast-selective ERFE loss resulted in enhanced erythropoietin receptor (\n                    <jats:italic toggle=\"yes\">Epor<\/jats:italic>\n                    ) and bone morphogenetic protein 4 (\n                    <jats:italic toggle=\"yes\">Bmp4<\/jats:italic>\n                    ) expression in whole bone in vivo and in osteoblasts ex vivo. Finally, the osteoblast-selective\n                    <jats:italic toggle=\"yes\">Erfe<\/jats:italic>\n                    mutants showed erythroid lineage proliferation and enhanced EPO responsiveness in a BMP4-dependent manner. Taken together, we posit that ERFE loss specifically from osteoblasts enhances RBC recovery during stress erythropoiesis\u2014defining mechanisms of regulation in the crosstalk between osteoblasts and erythroblasts.\n                  <\/jats:p>","DOI":"10.1073\/pnas.2537627123","type":"journal-article","created":{"date-parts":[[2026,4,28]],"date-time":"2026-04-28T17:59:57Z","timestamp":1777399197000},"update-policy":"https:\/\/doi.org\/10.1073\/pnas.cm10313","source":"Crossref","is-referenced-by-count":3,"title":["Erythroferrone derived from osteoblasts regulates stress erythropoiesis"],"prefix":"10.1073","volume":"123","author":[{"given":"Pinanong","family":"Na-Phatthalung","sequence":"first","affiliation":[{"name":"Division of Hematology and Medical Oncology, Tisch Cancer Institute, Icahn School of Medicine at Mount Sinai","place":["New York"]},{"name":"Institute for Translational Medicine and Pharmacology, Icahn School of Medicine at Mount Sinai","place":["New 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Deposited 10 April 2026."}],"container-title":["Proceedings of the National Academy of Sciences"],"original-title":[],"language":"en","link":[{"URL":"https:\/\/pnas.org\/doi\/pdf\/10.1073\/pnas.2537627123","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2026,4,28]],"date-time":"2026-04-28T18:00:47Z","timestamp":1777399247000},"score":1,"resource":{"primary":{"URL":"https:\/\/pnas.org\/doi\/10.1073\/pnas.2537627123"}},"subtitle":[],"short-title":[],"issued":{"date-parts":[[2026,4,28]]},"references-count":31,"journal-issue":{"issue":"18","published-print":{"date-parts":[[2026,5,5]]}},"alternative-id":["10.1073\/pnas.2537627123"],"URL":"https:\/\/doi.org\/10.1073\/pnas.2537627123","relation":{},"ISSN":["0027-8424","1091-6490"],"issn-type":[{"value":"0027-8424","type":"print"},{"value":"1091-6490","type":"electronic"}],"subject":[],"published":{"date-parts":[[2026,4,28]]},"assertion":[{"value":"2025-12-24","order":0,"name":"received","label":"Received","group":{"name":"publication_history","label":"Publication History"}},{"value":"2026-03-13","order":2,"name":"accepted","label":"Accepted","group":{"name":"publication_history","label":"Publication History"}},{"value":"2026-04-28","order":3,"name":"published","label":"Published","group":{"name":"publication_history","label":"Publication History"}}],"article-number":"e2537627123"}}