Evidence map›Paper›PMID 26846448›Full record

ReviewBritish journal of haematology2016

Advances in understanding erythropoiesis: evolving perspectives.

Satish K Nandakumar, Jacob C Ulirsch, Vijay G Sankaran

Abstract readReview
In one paragraph

Review in British journal of haematology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 88 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
88citing papers in PubMed, 1 pooled it
–field-weighted citation impact
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

88 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. Article
  3. Thalassaemia.Nature reviews. Disease primers · 2026
    Review
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  20. Frontiers in immunology · 2025
    Review

28 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

3 authors.

Satish K NandakumarDivision of Hematology/Oncology, The Manton Center for Orphan Disease Research, Boston Children's Hospital and Department of Pediatric Oncology, Dana-Farber Cancer Institute, Harvard Medical School, Boston, MA, USA.
Jacob C UlirschDivision of Hematology/Oncology, The Manton Center for Orphan Disease Research, Boston Children's Hospital and Department of Pediatric Oncology, Dana-Farber Cancer Institute, Harvard Medical School, Boston, MA, USA.
Vijay G SankaranDivision of Hematology/Oncology, The Manton Center for Orphan Disease Research, Boston Children's Hospital and Department of Pediatric Oncology, Dana-Farber Cancer Institute, Harvard Medical School, Boston, MA, USA.

Funding

Translational and clinical studies targeting y-globin modulationU01HL117720 · NHLBI · BOSTON CHILDREN'S HOSPITAL · PI SANKARAN, VIJAY GANESH · 2013 to 2017
$7.4M
Systematic Genetic Dissection of Human ErythropoiesisR01DK103794 · NIDDK · BOSTON CHILDREN'S HOSPITAL · PI Vijay Ganesh Sankaran · 2014 to 2026
$5.9M
Identifying Genome-wide Association Study-Nominated Regulators of ErythropoiesisR21HL120791 · NHLBI · BOSTON CHILDREN'S HOSPITAL · PI SANKARAN, VIJAY GANESH · 2014 to 2015
$477k
NHLBI NIH HHS R21 HL120791NHLBI NIH HHS U01 HL117720NIDDK NIH HHS R01 DK103794
6 · The paper itself

Abstract

Red blood cells (RBCs) are generated from haematopoietic stem and progenitor cells (HSPCs) through the step-wise process of differentiation known as erythropoiesis. In this review, we discuss our current understanding of erythropoiesis and highlight recent advances in this field. During embryonic development, erythropoiesis occurs in three distinct waves comprising first, the yolk sac-derived primitive RBCs, followed sequentially by the erythro-myeloid progenitor (EMP) and HSPC-derived definitive RBCs. Recent work has highlighted the complexity and variability that may exist in the hierarchical arrangement of progenitors responsible for erythropoiesis. Using recently defined cell surface markers, it is now possible to enrich for erythroid progenitors and precursors to a much greater extent than has been possible before. While a great deal of knowledge has been gained on erythropoiesis from model organisms, our understanding of this process is currently being refined through human genetic studies. Genes mutated in erythroid disorders can now be identified more rapidly by the use of next-generation sequencing techniques. Genome-wide association studies on erythroid traits in healthy populations have also revealed new modulators of erythropoiesis. All of these recent developments have significant promise not only for increasing our understanding of erythropoiesis, but also for improving our ability to intervene when RBC production is perturbed in disease.

Indexed as

AnimalsCell CommunicationCell DifferentiationEmbryonic DevelopmentErythropoiesisHematologic DiseasesHematopoietic Stem CellsHemoglobinsHeterograftsHumansMiceModels, BiologicalTranscription, GeneticZebrafishHemoglobinserythropoiesishaematopoiesishaemopoietic progenitorsred cell disordersred cells

Identifiers

PMID26846448
PMCPMC4833665

What OpenQuestion holds

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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.