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. 2020 Aug 4;7(19):2000383. doi: 10.1002/advs.202000383

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© 2020 The Authors. Published by Wiley‐VCH GmbH

This is an open access article under the terms of the http://creativecommons.org/licenses/by/4.0/ License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.

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Roles of hypo‐produced EPO in the anemia‐related detrimental effects on the bone under heavy metal exposure. The renal hypoproduction of EPO is induced by heavy metals. EPO deficiency impairs osteogenesis by downregulating several key signaling pathways in osteoblasts and/or osteoblasts/HSCs. Upon EPO deficiency, post‐traumatic inflammation is enhanced, and angiogenesis is impaired during bone healing. Additionally, EPO deficiency fails to induce vascular endothelial growth factor (VEGF) expression and increase peripheral endothelial progenitor cells. EPO, erythropoietin; HSC, hematopoietic stem cell; MSC, mesenchymal stem cell; JAK2, Janus kinase 2; mTOR, mechanistic target of rapamycin; PI3K, phosphoinositide 3‐kinase; BMP2, bone morphogenetic protein 2.