Evidence map›Paper›PMID 26283707›Full record

ReviewExperimental biology and medicine (Maywood, N.J.)2015

Cell signaling pathways involved in drug-mediated fetal hemoglobin induction: Strategies to treat sickle cell disease.

Betty S Pace, Li Liu, Biaoru Li, Levi H Makala

Open access · greenAbstract readReview
In one paragraph

Review in Experimental biology and medicine (Maywood, N.J.), 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
1.6field-weighted citation impact, top 18% 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

12 citing papers in PubMed, 25 citations in OpenAlex.

  1. Review
  2. Review
  3. Current status of beta-thalassemia and its treatment strategies.Molecular genetics & genomic medicine · 2021
    Review
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Review
  10. SIRT1 activates the expression of fetal hemoglobin genes.American journal of hematology · 2017
    Article
  11. Review
  12. Article
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.

Betty S PaceDepartment of Pediatrics, Georgia Regents University, Augusta, GA 30912, USA Department of Biochemistry and Molecular Biology, Georgia Regents University, Augusta, GA 30912, USA bpace@gru.edu.
Li LiuDepartment of Biological Sciences, University of Texas at Dallas, Richardson, TX 75083, USA.
Biaoru LiDepartment of Pediatrics, Georgia Regents University, Augusta, GA 30912, USA.
Levi H MakalaDepartment of Pediatrics, Georgia Regents University, Augusta, GA 30912, USA.
Augusta University · USThe University of Texas at Dallas · US

Funding

Mechanisms For p38 MAP Kinase DependentT Gene InductionR01HL069234 · NHLBI · UNIVERSITY OF TEXAS DALLAS · PI PACE, BETTY SUE · 2001 to 2017
$4.6M
NHLBI NIH HHS HL69234NHLBI NIH HHS R01 HL069234
6 · The paper itself

Abstract

The developmental regulation of globin gene expression has shaped research efforts to establish therapeutic modalities for individuals affected with sickle cell disease and β-thalassemia. Fetal hemoglobin has been shown to block sickle hemoglobin S polymerization to improve symptoms of sickle cell disease; moreover, fetal hemoglobin functions to replace inadequate hemoglobin A synthesis in β-thalassemia thus serving as an effective therapeutic target. In the perinatal period, fetal hemoglobin is synthesized at high levels followed by a decline to adult levels by one year of age. It is known that naturally occurring mutations in the γ-globin gene promoters and distant cis-acting transcription factors produce persistent fetal hemoglobin synthesis after birth to ameliorate clinical symptoms. Major repressor proteins that silence γ-globin during development have been targeted for gene therapy in β-hemoglobinopathies patients. In parallel effort, several classes of pharmacological agents that induce fetal hemoglobin expression through molecular and cell signaling mechanisms have been identified. Herein, we reviewed the progress made in the discovery of signaling molecules targeted by pharmacologic agents that enhance γ-globin expression and have the potential for future drug development to treat the β-hemoglobinopathies.

Indexed as

AgingAnemia, Sickle Cellbeta-ThalassemiaFetal HemoglobinHumansSignal TransductionFetal Hemoglobincell signalingFetal hemoglobinNRF2p38 MAPKsickle cell diseaseβ-hemoglobinopathies

Identifiers

PMID26283707
PMCPMC4935285
OpenAlexW1921966331

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.