Evidence map›Paper›PMID 28151426›Full record

ArticleBlood2017

Decreasing TfR1 expression reverses anemia and hepcidin suppression in β-thalassemic mice.

Huihui Li, Tenzin Choesang, Weili Bao, Huiyong Chen, Maria Feola, Daniel Garcia-Santos, Jie Li, Shuming Sun, Antonia Follenzi, Petra Pham and 9 more

Erratum issuedOpen access · bronzeAbstract read
In one paragraph

Article in Blood, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 42 papers.

0numbers the graph read from it
0cells of the map it votes in
42citing papers in PubMed
4.9field-weighted citation impact, top 4% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

42 citing papers in PubMed, 73 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Review
  5. Iron-Loading Anemias.Advances in experimental medicine and biology · 2025
    Review
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  7. Article
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  19. β-Thalassemia: evolving treatment options beyond transfusion and iron chelation.Hematology. American Society of Hematology. Education Program · 2021
    Review
  20. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

19 authors at 7 institutions in 4 countries.

Huihui LiHunan Key Laboratory of Carcinogenesis and Cancer Invasion, Cancer Research Institute, Central South University, Ministry of Education, Changsha, China.
Tenzin ChoesangErythropoiesis Laboratory, New York Blood Center, New York, NY.
Weili BaoErythropoiesis Laboratory, New York Blood Center, New York, NY.
Huiyong ChenErythropoiesis Laboratory, New York Blood Center, New York, NY.
Maria FeolaDivision of Hematology and Medical Oncology, Icahn School of Medicine at Mount Sinai, New York, NY.
Daniel Garcia-SantosJewish General Hospital, Lady Davis Institute, McGill University, Montreal, QC, Canada.
Jie LiLaboratory of Membrane Biology, New York Blood Center, New York, NY.
Shuming SunErythropoiesis Laboratory, New York Blood Center, New York, NY.
Antonia FollenziUniversity of Piemonte Orientale, Amedeo Avogadro, Novara, Italy.
Petra PhamFlow Cytometry Core Laboratory, Lindsley F. Kimball Research Institute, New York Blood Center, New York, NY.
Jing LiuState Key Laboratory of Medical Genetics and School of Life Sciences, Central South University, Changsha, China.
Jinghua ZhangLaboratory of Membrane Biology, New York Blood Center, New York, NY.
Prem PonkaJewish General Hospital, Lady Davis Institute, McGill University, Montreal, QC, Canada.
Xiuli AnLaboratory of Membrane Biology, New York Blood Center, New York, NY.
Narla MohandasLaboratory of Membrane Biology, New York Blood Center, New York, NY.
Robert E FlemingSaint Louis University, Saint Louis, MO; and.
Stefano RivellaChildren's Hospital of Philadelphia, Philadelphia, PA.
Guiyuan LiHunan Key Laboratory of Carcinogenesis and Cancer Invasion, Cancer Research Institute, Central South University, Ministry of Education, Changsha, China.
Yelena Z GinzburgHunan Key Laboratory of Carcinogenesis and Cancer Invasion, Cancer Research Institute, Central South University, Ministry of Education, Changsha, China.
New York Blood Center · USCentral South University · CNIcahn School of Medicine at Mount Sinai · USJewish General Hospital · CAChildren's Hospital of Philadelphia · USSaint Louis University · USUniversità degli Studi del Piemonte Orientale “Amedeo Avogadro” · IT

Funding

Regulatory Role of Transferrin in Erythropoiesis and Iron MetabolismR01DK095112 · NIDDK · SAINT LOUIS UNIVERSITY · PI Robert E Fleming, Yelena Ginzburg · 2012 to 2026
$5.4M
Hepcidin therapy for iron overload and hematologic disordersR01DK090554 · NIDDK · WEILL MEDICAL COLL OF CORNELL UNIV · PI RIVELLA, STEFANO · 2010 to 2021
$5.2M
The Role of Erythroferrone in Regulating Bone Metabolism in Beta-ThalassemiaR01DK107670 · NIDDK · NEW YORK BLOOD CENTER · PI GINZBURG, YELENA, YUEN, TONY · 2015 to 2025
$4.5M
Understanding and Improving Iron Distribution and Erythropoiesis in Beta-ThalasseK08HL105682 · NHLBI · NEW YORK BLOOD CENTER · PI GINZBURG, YELENA · 2011 to 2015
$661k
NHLBI NIH HHS K08 HL105682NIDDK NIH HHS R01 DK090554NIDDK NIH HHS R01 DK095112NIDDK NIH HHS R01 DK107670
6 · The paper itself

Abstract

Iron availability for erythropoiesis and its dysregulation in β-thalassemia are incompletely understood. We previously demonstrated that exogenous apotransferrin leads to more effective erythropoiesis, decreasing erythroferrone (ERFE) and derepressing hepcidin in β-thalassemic mice. Transferrin-bound iron binding to transferrin receptor 1 (TfR1) is essential for cellular iron delivery during erythropoiesis. We hypothesize that apotransferrin's effect is mediated via decreased TfR1 expression and evaluate TfR1 expression in β-thalassemic mice in vivo and in vitro with and without added apotransferrin. Our findings demonstrate that β-thalassemic erythroid precursors overexpress TfR1, an effect that can be reversed by the administration of exogenous apotransferrin. In vitro experiments demonstrate that apotransferrin inhibits TfR1 expression independent of erythropoietin- and iron-related signaling, decreases TfR1 partitioning to reticulocytes during enucleation, and enhances enucleation of defective β-thalassemic erythroid precursors. These findings strongly suggest that overexpressed TfR1 may play a regulatory role contributing to iron overload and anemia in β-thalassemic mice. To evaluate further, we crossed TfR1

Indexed as

AnemiaAnimalsApoproteinsbeta-ThalassemiaErythropoiesisHepcidinsIron OverloadMiceReceptors, TransferrinTransferrinApoproteinsapotransferrinHepcidinsReceptors, TransferrinTfrc protein, mouseTransferrin

Identifiers

PMID28151426
PMCPMC5356456
OpenAlexW2585591789

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.