Evidence map›Paper›PMID 26226206›Full record

ReviewTranslational research : the journal of laboratory and clinical medicine2016

Inflammatory targets of therapy in sickle cell disease.

Amma Owusu-Ansah, Chibueze A Ihunnah, Aisha L Walker, Solomon F Ofori-Acquah

Open access · greenAbstract readReview
In one paragraph

Review in Translational research : the journal of laboratory and clinical medicine, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
2.2field-weighted citation impact, top 13% 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

24 citing papers in PubMed, 43 citations in OpenAlex.

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  17. Modulating NRF2 in Disease: Timing Is Everything.Annual review of pharmacology and toxicology · 2019
    Review
  18. New insights into the pathophysiology and development of novel therapies for sickle cell disease.Hematology. American Society of Hematology. Education Program · 2018
    Review
  19. Article
  20. 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 1 institution in 1 country.

Amma Owusu-AnsahDivision of Hematology, Department of Medicine, University of Pittsburgh, Pittsburgh, PA; Center for Translational and International Hematology, Heart, Lung and Blood Vascular Medicine Institute, University of Pittsburgh, Pittsburgh, PA.
Chibueze A IhunnahCenter for Translational and International Hematology, Heart, Lung and Blood Vascular Medicine Institute, University of Pittsburgh, Pittsburgh, PA; Division of Pulmonary Medicine, Department of Medicine, University of Pittsburgh, Pittsburgh, PA.
Aisha L WalkerCenter for Translational and International Hematology, Heart, Lung and Blood Vascular Medicine Institute, University of Pittsburgh, Pittsburgh, PA; Division of Pulmonary Medicine, Department of Medicine, University of Pittsburgh, Pittsburgh, PA.
Solomon F Ofori-AcquahDivision of Hematology, Department of Medicine, University of Pittsburgh, Pittsburgh, PA; Center for Translational and International Hematology, Heart, Lung and Blood Vascular Medicine Institute, University of Pittsburgh, Pittsburgh, PA; Division of Pulmonary Medicine, Department of Medicine, University of Pittsburgh, Pittsburgh, PA. Electronic address: sfo2@pitt.edu.
University of Pittsburgh · US

Funding

Cellular and Molecular Mechanisms of Acute Lung Injury in Sickle Cell DiseaseU01HL117721 · NHLBI · EMORY UNIVERSITY · PI DEBAUN, MICHAEL R., JOINER, CLINTON H · 2013 to 2017
$9.4M
Translational Pulmonary Vascular BiologyT32HL110849 · NHLBI · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI Sruti Shiva · 2012 to 2026
$5.0M
Mechanisms of endothelial barrier phenotypes in sickle cell diseaseR01HL106192 · NHLBI · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI OFORI-ACQUAH, SOLOMON FIIFI · 2011 to 2016
$2.1M
NHLBI NIH HHS R01 HL106192NHLBI NIH HHS R01HL106192NHLBI NIH HHS T32 HL110849NHLBI NIH HHS U01 HL117721NHLBI NIH HHS U01HL117721
6 · The paper itself

Abstract

Sickle cell disease (SCD) is a monogenic globin disorder characterized by the production of a structurally abnormal hemoglobin (Hb) variant Hb S, which causes severe hemolytic anemia, episodic painful vaso-occlusion, and ultimately end-organ damage. The primary disease pathophysiology is intracellular Hb S polymerization and consequent sickling of erythrocytes. It has become evident for more than several decades that a more complex disease process contributes to the myriad of clinical complications seen in patients with SCD with inflammation playing a central role. Drugs targeting specific inflammatory pathways therefore offer an attractive therapeutic strategy to ameliorate many of the clinical events in SCD. In addition, they are useful tools to dissect the molecular and cellular mechanisms that promote individual clinical events and for developing improved therapeutics to address more challenging clinical dilemmas such as refractoriness to opioids or hyperalgesia. Here, we discuss the prospect of targeting multiple inflammatory pathways implicated in the pathogenesis of SCD with a focus on new therapeutics, striving to link the actions of the anti-inflammatory agents to a defined pathobiology, and specific clinical manifestations of SCD. We also review the anti-inflammatory attributes and the cognate inflammatory targets of hydroxyurea, the only Food and Drug Administration-approved drug for SCD.

Indexed as

Anemia, Sickle CellAnimalsAnti-Inflammatory AgentsHumansHydroxyureaInflammationSignal TransductionAnti-Inflammatory AgentsHydroxyurea

Identifiers

PMID26226206
PMCPMC4684475
OpenAlexW868376623

What OpenQuestion holds

Textmetadata
LicenceTDM
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.