Evidence map›Paper›PMID 28378932›Full record

ReviewAmerican journal of hematology2017

The role of carbon monoxide and heme oxygenase in the prevention of sickle cell disease vaso-occlusive crises.

Edward Gomperts, John D Belcher, Leo E Otterbein, Thomas D Coates, John Wood, Brett E Skolnick, Howard Levy, Gregory M Vercellotti

Open access · bronzeAbstract readReview
In one paragraph

Review in American journal of hematology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
2.0field-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

25 citing papers in PubMed, 48 citations in OpenAlex.

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  9. Neuregulin-1 attenuates hemolysis- and ischemia induced-cerebrovascular inflammation associated with sickle cell disease.Journal of stroke and cerebrovascular diseases : the official journal of National Stroke Association · 2023
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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

8 authors at 4 institutions in 1 country.

Edward GompertsHillhurst Biopharmaceuticals, Inc, 2029 Verdugo Blvd., #125, Montrose, CA, 91020, USA.ORCID http://orcid.org/0000-0001-5904-265X
John D BelcherUniversity of Minnesota, 420 Delaware Street SE, MMC 480, Minneapolis, MN, 55455, USA.
Leo E OtterbeinHarvard Medical School; Beth Israel Deaconess Medical Center, 3 Blackfan Circle Center for Life Sciences, #630, Boston, MA, 02115, USA.
Thomas D CoatesChildren's Hospital Los Angeles; University of Southern California, 4650 Sunset Boulevard MS #54 Los Angeles, CA, 90027, USA.
John WoodChildren's Hospital Los Angeles; University of Southern California, 4650 Sunset Boulevard MS #54 Los Angeles, CA, 90027, USA.
Brett E SkolnickHillhurst Biopharmaceuticals, Inc, 2029 Verdugo Blvd., #125, Montrose, CA, 91020, USA.
Howard LevyHillhurst Biopharmaceuticals, Inc, 2029 Verdugo Blvd., #125, Montrose, CA, 91020, USA.
Gregory M VercellottiUniversity of Minnesota, 420 Delaware Street SE, MMC 480, Minneapolis, MN, 55455, USA.
Hillhurst Biopharmaceuticals (United States) · USUniversity of Minnesota · USUniversity of Southern California · USBeth Israel Deaconess Medical Center · US

Funding

Neuromodulatory Mechanisms and Regional Autonomic Dysregulation in the Development of Pain in Sickle Cell Disease PatientsU01HL117718 · NHLBI · CHILDREN'S HOSPITAL OF LOS ANGELES · PI COATES, THOMAS DUANE, KHOO, MICHAEL C K · 2013 to 2017
$9.6M
Heme toxicity and vaso-occlusion in sickle cell diseaseR01HL114567 · NHLBI · UNIVERSITY OF MINNESOTA · PI VERCELLOTTI, GREGORY M · 2012 to 2020
$4.4M
Oral Carbon Monoxide Therapeutic to Prevent Vaso-Occlusive Crises in Sickle Cell DiseaseR43HL131065 · NHLBI · HILLHURST BIOPHARMACEUTICALS, INC. · PI BELCHER, JOHN D, GOMPERTS, EDWARD · 2016 to 2017
$300k
NHLBI NIH HHS R01 HL114567NHLBI NIH HHS R43 HL131065NHLBI NIH HHS U01 HL117718
6 · The paper itself

Abstract

Sickle Cell Disease (SCD) is a painful, lifelong hemoglobinopathy inherited as a missense point mutation in the hemoglobin (Hb) beta-globin gene. This disease has significant impact on quality of life and mortality, thus a substantial medical need exists to reduce the vaso-occlusive crises which underlie the pathophysiology of the disease. The concept that a gaseous molecule may exert biological function has been well known for over one hundred years. Carbon monoxide (CO), although studied in SCD for over 50 years, has recently emerged as a powerful cytoprotective biological response modifier capable of regulating a host of physiologic and therapeutic processes that, at low concentrations, exerts key physiological functions in various models of tissue inflammation and injury. CO is physiologically generated by the metabolism of heme by the heme oxygenase enzymes and is measurable in blood. A substantial amount of preclinical and clinical data with CO have been generated, which provide compelling support for CO as a potential therapeutic in a number of pathological conditions. Data underlying the therapeutic mechanisms of CO, including in SCD, have been generated by a plethora of in vitro and preclinical studies including multiple SCD mouse models. These data show CO to have key signaling impacts on a host of metallo-enzymes as well as key modulating genes that in sum, result in significant anti-inflammatory, anti-oxidant and anti-apoptotic effects as well as vasodilation and anti-adhesion of cells to the endothelium resulting in preservation of vascular flow. CO may also have a role as an anti-polymerization HbS agent. In addition, considerable scientific data in the non-SCD literature provide evidence for a beneficial impact of CO on cerebrovascular complications, suggesting that in SCD, CO could potentially limit these highly problematic neurologic outcomes. Research is needed and hopefully forthcoming, to carefully elucidate the safety and benefits of this potential therapy across the age spectrum of patients impacted by the host of pathophysiological complications of this devastating disease.

Indexed as

Anemia, Sickle CellAnimalsCarbon MonoxideClinical Trials as TopicDisease Models, AnimalHeme Oxygenase (Decyclizing)HemoglobinsHumansSignal TransductionTreatment OutcomeVascular DiseasesCarbon MonoxideHeme Oxygenase (Decyclizing)Hemoglobins

Identifiers

PMID28378932
PMCPMC5723421
OpenAlexW2604159311

What OpenQuestion holds

Textmetadata
LicenceTDM
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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.