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Erythropoietin administration in humans causes a marked and prolonged reduction in circulating hepcidin
Open accessAbstract
Expression of hepcidin, the key hormone governing iron transport, is reduced by anemia in a manner which appears dependent on increased bone marrow activity. The temporal associations between plasma hepcidin and other iron parameters were examined in healthy humans after erythropoietin administration and venesection. Profound hepcidin suppression appeared abruptly 24 hours after subcutaneous erythropoietin (P=0.003), and was near maximal at onset, with peak (mid-afternoon) levels reduced by 73.2%, gradually recovering over the following two weeks. Minor changes in circulating iron, soluble transferrin receptor and growth differentiation factor-15 were observed after the reduction in hepcidin. Similar but more gradual changes in these parameters were observed after reducing hematocrit by removal of 250 mL blood. These human studies confirm the importance of a rapidly responsive marrow-hepcidin axis in regulating iron supply in vivo, and suggest that this axis is regulated by factors other than circulating iron, soluble transferrin receptor or growth differentiation factor-15.
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“studies in humans receiving recombinant EPO have not yet shown a significant inverse relationship between serum hepcidin and GDF15 levels”
From Regulation of erythropoiesis by hypoxia-inducible factors (2013) · cites this paper as [222]
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Cites
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An overview of molecular basis of iron metabolism regulation and the associated pathologies
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Zhao, N., Zhang, A., & Enns, C. A. (2013) · Journal of Clinical Investigation · doi:10.1172/jci67225 · Cited by 215
“However, in healthy humans, iron deficiency or reduced hepcidin expression caused by blood loss was not associated with elevated serum GDF15 (84, 85).”
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Múñoz, M., García‐Erce, J. A., & Remacha, A. F. (2010) · Journal of Clinical Pathology · doi:10.1136/jcp.2010.079046 · Cited by 206
“A recent study showed that EPO administration in humans causes a marked and prolonged reduction in circulating hepcidin.”
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Ganz, T., & Nemeth, E. (2016) · Seminars in Nephrology · doi:10.1016/j.semnephrol.2016.02.001 · Cited by 195
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Role of hepcidin in the pathophysiology and diagnosis of anemia
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Gluba-Brzózka, A., Franczyk, B., Olszewski, R., & Rysz, J. (2020) · International Journal of Molecular Sciences · doi:10.3390/ijms21030725 · Cited by 192
The Hepcidin-Ferroportin System as a Therapeutic Target in Anemias and Iron Overload Disorders
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Hypoxia induced downregulation of hepcidin is mediated by platelet derived growth factor BB
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BackgroundSystemic iron homeostasis and erythropoiesis
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BackgroundIron deficiency syndromes and iron‐restricted erythropoiesis (CME)
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“, myelodysplastic syndromes or hemolytic anemias) suppress hepcidin to very low levels.(49,50) Low hepcidin allows increased absorption of dietary iron and release of iron storage.”
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“In fact, EPO injections in mice and humans resulted in suppression of hepcidin production [92,93], and this may be the mechanism by which high EPO levels overcome iron restriction.”
Lin, D. M.-H., Lin, E. S., & Tran, M. (2013) · Transfusion Medicine Reviews · doi:10.1016/j.tmrv.2013.09.001 · Cited by 116
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“poietic stimulus results in a sustained decrease of serum hepcidin concentration that begins within hours [30, 31].”
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Petzer, V., Theurl, I., & Weiß, G. (2018) · Pharmaceuticals · doi:10.3390/ph11040135 · Cited by 41
“Notably, EPO at high doses can decrease hepcidin levels [176].”
BackgroundBanfi, G., Lombardi, G., Colombini, A., & Lippi, G. (2010) · Clinica Chimica Acta · doi:10.1016/j.cca.2010.03.039 · Cited by 40
Hepcidin is a Potential Regulator of Iron Status in Chronic Kidney Disease
Tsuchiya, K., & Nitta, K. (2012) · Therapeutic Apheresis and Dialysis · doi:10.1111/1744-9987.12001 · Cited by 42
“Regulation by erythropoietic signals Administration of erythropoiesis-stimulating agents (ESAs) has been found to decrease hepcidin production by hepatocytes (30,40,41).”
BackgroundWagner, M., Ashby, D. R., Kurtz, C. B., Alam, A., Busbridge, M., Raff, U., Zimmermann, J., Heuschmann, P. U., Wanner, C., & Schramm, L. (2015) · PLoS ONE · doi:10.1371/journal.pone.0123072 · Cited by 42
Advancements in anemias related to chronic conditions
Guidi, G. C., & Santonastaso, C. L. (2010) · Clinical Chemistry and Laboratory Medicine (CCLM) · doi:10.1515/cclm.2010.264 · Cited by 39
Iron: The new advances in therapy
Auerbach, M., Goodnough, L. T., & Shander, A. (2013) · Best practice & research. Clinical anaesthesiology · doi:10.1016/j.bpa.2012.12.001 · Cited by 37
Hennigar, S. R., Berryman, C. E., Harris, M. N., Karl, J. P., Lieberman, H. R., McClung, J. P., Rood, J. C., & Pasiakos, S. M. (2020) · The Journal of Clinical Endocrinology & Metabolism · doi:10.1210/clinem/dgz316 · Cited by 36
Erythropoietic drive is the strongest predictor of hepcidin level in adults with sickle cell disease
Karafin, M. S., Koch, K. L., Rankin, A. B., Nischik, D., Rahhal, G., Simpson, P. M., & Field, J. J. (2015) · Blood Cells Molecules and Diseases · doi:10.1016/j.bcmd.2015.07.010 · Cited by 36
Investigational therapies for renal disease-induced anemia
Schmid, H., & JELKMANN, W. E. B. (2016) · Expert Opinion on Investigational Drugs · doi:10.1080/13543784.2016.1182981 · Cited by 33
“Despite beneficial hepcidin-lowering effects in animal models and in humans for, for example, heparin application, alcohol loading[109], ESA treatment, [110] or vitamin D administration [111], none of these options will be able to definitely lower increased hepcidin levels in CKD patients.”
BackgroundLiver iron modulates hepcidin expression during chronically elevated erythropoiesis in mice
Díaz, V., Gammella, E., Recalcati, S., Santambrogio, P., Naldi, A. M., Vogel, J., Gassmann, M., & Cairo, G. (2013) · Hepatology · doi:10.1002/hep.26550 · Cited by 33
Iron and oxygen sensing: a tale of 2 interacting elements?
Simpson, R. J., & McKie, A. T. (2014) · Metallomics · doi:10.1039/c4mt00225c · Cited by 32
Govus, A. D., Abbiss, C. R., Garvican‐Lewis, L. A., Swinkels, D. W., Laarakkers, C. M., Gore, C. J., & Peeling, P. (2014) · European Journal of Applied Physiology · doi:10.1007/s00421-014-2938-2 · Cited by 30
Keel, S., Doty, R. T., Liu, L., Nemeth, E., Cherian, S., Ganz, T., & Abkowitz, J. L. (2015) · Experimental Hematology · doi:10.1016/j.exphem.2015.03.001 · Cited by 29
“We favor the possibility that Tfrc functions as a signaling molecule because the alternative possibility, that soluble Tfrc (released from erythroid cells) directly suppresses liver hepcidin expression, is inconsistent with published work [15,35,36] and our data in Tfrc+/− mice.”
BackgroundResultTreatment of renal anemia: Erythropoiesis stimulating agents and beyond
Biggar, P. H., & Kim, G. (2017) · Kidney Research and Clinical Practice · doi:10.23876/j.krcp.2017.36.3.209 · Cited by 31
“However, conventional ESAs offer a comprehensive safety profile which should be the future comparison standard for the newer substance classes.”
BackgroundInfluentialMechanisms and Regulation of Intestinal Iron Transport
Collins, J. F., Flores, S. R., Wang, X., & Anderson, G. J. (2018) · Elsevier eBooks · doi:10.1016/b978-0-12-809954-4.00060-8 · Cited by 30
Mojzíková, R., Kořalková, P., Holub, D., Zidova, Z., Pospíšilová, D., Čermák, J., Striezencova, Z. L., Indrák, K., Suková, M., Partschova, M., et al. (2014) · British Journal of Haematology · doi:10.1111/bjh.12779 · Cited by 29
“Candidate erythroid signals regulating hepcidin To clarify the involvement of erythropoiesis in iron metabolism in PK deficiency, serum levels of GDF15 and EPO, two markers of erythropoietic activity known to be associated with hepcidin production, were evaluated.”
BackgroundInfluentialLainé, F., Laviolle, B., Ropert, M., Bouguen, G., Morçet, J., Hamon, C., Massart, C., Westermann, M., Deugnier, Y., & Loréal, O. (2011) · European Journal of Applied Physiology · doi:10.1007/s00421-011-2097-7 · Cited by 26
Lehmberg, K., Grosse, R., Muckenthaler, M. U., Altamura, S., Nielsen, P., Schmid, H., Graubner, U. B., Oyen, F., Zeller, W., Schneppenheim, R., et al. (2012) · Annals of Hematology · doi:10.1007/s00277-012-1618-8 · Cited by 25
“As erythropoietin (EPO) has been shown to decrease plasma hepcidin in healthy individuals [10], recombinant human EPO may constitute a potential remedy for IRIDA patients.”
BackgroundTarkun, P., Mehtap, Ö., Ateşoğlu, E. B., Gedük, A., Musul, M. M., & Hacıhanefioğlu, A. (2013) · European Journal Of Haematology · doi:10.1111/ejh.12150 · Cited by 26
“On the other hand, studies in patients with effective erythropoiesis after bone marrow transplantation or after injection of erythropoietin failed to demonstrate major increases in serum GDF-15 (18, 19).”
BackgroundRobach, P., Recalcati, S., Girelli, D., Campostrini, N., Kempf, T., Wollert, K. C., Corbella, M., Santambrogio, P., Perbellini, L., Brasse‐Lagnel, C., et al. (2013) · European Journal Of Haematology · doi:10.1111/ejh.12122 · Cited by 25
“However, the fact that 1) GDF-15 levels were still within the normal range and well below the levels necessary to repress hepcidin mRNA expression in human hepatic cells (9), and 2) low-dose Epo blunted hepcidin expression without noticeable GDF-15 changes [(23, 24) and present study] argues against GDF-15 as a putati…”
BackgroundResultInfluentialIron Mining for Erythropoiesis
Correnti, M., Gammella, E., Cairo, G., & Recalcati, S. (2022) · International Journal of Molecular Sciences · doi:10.3390/ijms23105341 · Cited by 30
“Initial studies showing (1) strong downregulation of hepcidin in mice injected with EPO [18,52,73], (2) inhibition of hepcidin transcription in EPO-treated cell lines [74,75] and (3) a prompt decrease in hepcidin levels [76,77] that preceded any significant change in potential mediators following EPO administration to…”
ResultBone marrow iron distribution, hepcidin, and ferroportin expression in renal anemia
Bârsan, L., Stanciu, A., Stancu, S. H., Căpuşă, C. S., Brătescu, L., Mandache, E., Radu, E., & Mircescu, G. (2015) · Hematology · doi:10.1179/1607845415y.0000000004 · Cited by 24
Hepcidin and Erythropoietin Level in Sickle Cell Disease
Johnkennedy, N., Uche, U. B., Udujih, H. I., Chidozie, N. J., Obeagu, E. I., & Oluchi, A.-A. (2015) · Journal of Advances in Medicine and Medical Research · doi:10.9734/bjmmr/2015/17480 · Cited by 23
“The alteration of hepcidin production affects the erythropoietic activity in humans [7,8].”
BackgroundSong, J. W., Soh, S., Shim, J., Lee, S. H., Lee, S. H., Kim, H.-B., Kim, M.-Y., & Kwak, Y. L. (2021) · Annals of Surgery · doi:10.1097/sla.0000000000005011 · Cited by 23
“Erythropoietin also reduced circulating hepcidin levels 24 hour after subcutaneous administration in healthy humans.(23) In the study of Spahn et al,(24) concomitant erythropoietin treatment with intravenous iron 1 day before surgery resulted in increase of hemoglobin and reticulocyte from the day after surgery, sugge…”
BackgroundOlivera, J. D., Zhang, V., Nemeth, E., & Ganz, T. (2023) · Blood Advances · doi:10.1182/bloodadvances.2022009307 · Cited by 25
Signaling pathways regulating hepcidin
Rishi, G., & Subramaniam, V. N. (2019) · Vitamins and hormones · doi:10.1016/bs.vh.2019.01.003 · Cited by 23
HDAC1 governs iron homeostasis independent of histone deacetylation in iron-overload murine models
Yin, X., Wu, Q., Monga, J., Xie, E., Wang, H., Wang, S., Zhang, H., Wang, Z.-Y., Zhou, T., Shi, Y., et al. (2018) · Antioxidants & Redox Signaling · doi:10.1089/ars.2017.7161 · Cited by 22
Hepcidin in chronic kidney disease anemia
Santos‐Silva, A., Ribeiro, S., Reis, F., & Belo, L. (2019) · Vitamins and hormones · doi:10.1016/bs.vh.2019.01.012 · Cited by 23
Prolyl hydroxylase inhibitor desidustat improves anemia in erythropoietin hyporesponsive state
Joharapurkar, A. A., Patel, V. J., Kshirsagar, S. G., Patel, M. S., Savsani, H. H., Kajavadara, C. K., Valani, D., & Jain, M. R. (2022) · Current Research in Pharmacology and Drug Discovery · doi:10.1016/j.crphar.2022.100102 · Cited by 21
Elsewefy, D. A., Farweez, B. A. T., Behairy, M., & Yassin, N. R. (2019) · International Urology and Nephrology · doi:10.1007/s11255-018-2062-z · Cited by 22
Hematologic Aspects of Kidney Disease
Brugnara, C., & Eckardt, K. (2012) · Elsevier eBooks · doi:10.1016/b978-1-4160-6193-9.10056-9 · Cited by 21
Coe, C. L., Lubach, G. R., Busbridge, M., & Chapman, R. (2013) · Research in Veterinary Science · doi:10.1016/j.rvsc.2012.11.017 · Cited by 20
“Prior comparisons had verified that Hep-25 values determined by this RIA were highly correlated with established SELDI-TOF-Mass Spectrometry methods (r = 0.96) (Ashby et al., 2010).”
Influential
Metadata
- Authors
- Ashby, D. R., Gale, D. P., Busbridge, M., Murphy, K. G., Duncan, N. D., Cairns, T. D., Taube, D. H., Bloom, S. R., Tam, F. W. K., Chapman, R., Maxwell, P. H., & Choi, P.
- Affiliations
- Hammersmith Hospital (GB)
- University College London (GB)
- Imperial College London (GB)
- Venue
- Haematologica
- Published
- 2009-10-14
- Volume
- 95
- Issue
- 3
- Pages
- 505-508
- ISSN
- 0390-6078 (ISSN-L)
- 1592-8721
- PMC
- PMC2833083
- OpenAlex
- W2034565548
- Cited by
- 191
- References
- 26
- Citations by year
- 2026: 1 · 2025: 3 · 2024: 9 · 2023: 7 · 2022: 8 · 2021: 6 · 2020: 8 · 2019: 10 · 2018: 8 · 2017: 14 · 2016: 11 · 2015: 16 · 2014: 21 · 2013: 21 · 2012: 16
- FWCI
- 10.44
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Locations
- Haematologica (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion)
- Funders
- Wellcome Trust
- National Institute for Health and Care Research (NF-SI-0507-10315)
- Medical Research Council
- Topics
- Health Sciences › Medicine › Hematology › Iron Metabolism and Disorders
- Health Sciences › Medicine › Hematology › Erythropoietin and Anemia Treatment
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Biochemistry › Hemoglobin structure and function
- Keywords
- erythropoietin, hepcidin, iron metabolism, anemia, bone marrow, phlebotomy, soluble transferrin receptor, growth differentiation factor 15, hematocrit
- MeSH terms
- Adult, Bone Marrow, Erythropoietin, Humans, Injections, Subcutaneous, Iron, Male, Receptors, Transferrin, Transferrin, Antimicrobial Cationic Peptides, Growth Differentiation Factor 15, Hepcidins
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