Evidence map›Paper›PMID 30134792›Full record

ReviewMolecular medicine (Cambridge, Mass.)2018

Erythropoiesis: insights into pathophysiology and treatments in 2017.

Andrea Zivot, Jeffrey M Lipton, Anupama Narla, Lionel Blanc

Open access · goldAbstract readReview
In one paragraph

Review in Molecular medicine (Cambridge, Mass.), 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 64 papers.

0numbers the graph read from it
0cells of the map it votes in
64citing papers in PubMed
6.8field-weighted citation impact, top 2% 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

64 citing papers in PubMed, 148 citations in OpenAlex.

  1. Article
  2. High prevalence of molar-incisor hypomineralisation in sickle cell disease children and the association with haematologic profile: a retrospective cohort study.European archives of paediatric dentistry : official journal of the European Academy of Paediatric Dentistry · 2026
    Article
  3. Nucleated Red Blood Cells for Predicting Mortality in Intensive Care Unit Patients With Sepsis.Medical science monitor : international medical journal of experimental and clinical research · 2026
    Article
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  15. Article
  16. Article
  17. Review
  18. Iron-Loading Anemias.Advances in experimental medicine and biology · 2025
    Review
  19. Review
  20. Review

4 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

4 authors at 2 institutions in 1 country.

Andrea ZivotLaboratory of Developmental Erythropoiesis, Center for Autoimmune, Musculoskeletal, and Hematopoietic Diseases, The Feinstein Institute for Medical Research, 350 Community Drive, Manhasset, NY, 11030, USA.
Jeffrey M LiptonLaboratory of Developmental Erythropoiesis, Center for Autoimmune, Musculoskeletal, and Hematopoietic Diseases, The Feinstein Institute for Medical Research, 350 Community Drive, Manhasset, NY, 11030, USA.
Anupama NarlaDepartment of Molecular Medicine and Pediatrics, Donald and Barbara Zucker School of Medicine at Hofstra Northwell, Hempstead, NY, 11549, USA.
Lionel BlancLaboratory of Developmental Erythropoiesis, Center for Autoimmune, Musculoskeletal, and Hematopoietic Diseases, The Feinstein Institute for Medical Research, 350 Community Drive, Manhasset, NY, 11030, USA. Lblanc@northwell.edu.ORCID 0000-0002-0185-6260
Feinstein Institute for Medical Research · USDonald & Barbara Zucker School of Medicine at Hofstra/Northwell · US

Funding

Critical Regulatory Circuits in Blood FormationR01HL134043 · NHLBI · JACKSON LABORATORY · PI PETERS, LUANNE L · 2016 to 2019
$2.6M
NHLBI NIH HHS R01 HL134043
6 · The paper itself

Abstract

Erythropoiesis is a tightly-regulated and complex process originating in the bone marrow from a multipotent stem cell and terminating in a mature, enucleated erythrocyte.Altered red cell production can result from the direct impairment of medullary erythropoiesis, as seen in the thalassemia syndromes, inherited bone marrow failure as well as in the anemia of chronic disease. Alternatively, in disorders such as sickle cell disease (SCD) as well as enzymopathies and membrane defects, medullary erythropoiesis is not, or only minimally, directly impaired. Despite these differences in pathophysiology, therapies have traditionally been non-specific, limited to symptomatic control of anemia via packed red blood cell (pRBC) transfusion, resulting in iron overload and the eventual need for iron chelation or splenectomy to reduce defective red cell destruction. Likewise, in polycythemia vera overproduction of red cells has historically been dealt with by non-specific myelosuppression or phlebotomy. With a deeper understanding of the molecular mechanisms underlying disease pathophysiology, new therapeutic targets have been identified including induction of fetal hemoglobin, interference with aberrant signaling pathways and gene therapy for definitive cure. This review, utilizing some representative disorders of erythropoiesis, will highlight novel therapeutic modalities currently in development for treatment of red cell disorders.

Indexed as

ErythropoiesisAnimalsGenetic TherapyHematologic DiseasesHumansErythropoiesisRed cell disordersTherapy

Identifiers

PMID30134792
PMCPMC6016880
OpenAlexW2805210233

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.