Evidence map›Paper›PMID 32760278›Full record

ReviewFrontiers in pharmacology2020

Targeting the Heme Oxygenase 1/Carbon Monoxide Pathway to Resolve Lung Hyper-Inflammation and Restore a Regulated Immune Response in Cystic Fibrosis.

Caterina Di Pietro, Hasan H Öz, Thomas S Murray, Emanuela M Bruscia

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in pharmacology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed, 2 pooled it
1.9field-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

21 citing papers in PubMed, 2 syntheses or guidelines pooled it, 34 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
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  7. Article
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  10. The effect of extracorporeal shock wave on joint capsule fibrosis based on AJournal of orthopaedic surgery and research · 2023
    Article
  11. Review
  12. Review
  13. Review
  14. Cystic Fibrosis and Oxidative Stress: The Role of CFTR.Molecules (Basel, Switzerland) · 2022
    Review
  15. Article
  16. Review
  17. Review
  18. Article
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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

4 authors at 1 institution in 1 country.

Caterina Di PietroDepartment of Pediatrics, Yale University School of Medicine, New Haven, CT, United States.
Hasan H ÖzDepartment of Pediatrics, Yale University School of Medicine, New Haven, CT, United States.
Thomas S MurrayDepartment of Pediatrics, Yale University School of Medicine, New Haven, CT, United States.
Emanuela M BrusciaDepartment of Pediatrics, Yale University School of Medicine, New Haven, CT, United States.
Yale University · US

Funding

Yale Cooperative Hematology Specialized Core CenterU54DK106857 · NIDDK · YALE UNIVERSITY · PI JOHN HWA, Diane S Krause · 2015 to 2026
$9.7M
Yale Center of Excellence in Molecular HematologyP30DK072442 · NIDDK · YALE UNIVERSITY · PI KRAUSE, DIANE S · 2005 to 2010
$5.2M
CFTR and Toll-Like Receptor SignalingR01HL123851 · NHLBI · YALE UNIVERSITY · PI BRUSCIA, EMANUELA MARINA · 2016 to 2019
$1.7M
NHLBI NIH HHS R01 HL123851NIDDK NIH HHS P30 DK072442NIDDK NIH HHS U54 DK106857
6 · The paper itself

Abstract

In individuals with cystic fibrosis (CF), lung hyper-inflammation starts early in life and is perpetuated by mucus obstruction and persistent bacterial infections. The continuous tissue damage and scarring caused by non-resolving inflammation leads to bronchiectasis and, ultimately, respiratory failure. Macrophages (MΦs) are key regulators of immune response and host defense. We and others have shown that, in CF, MΦs are hyper-inflammatory and exhibit reduced bactericidal activity. Thus, MΦs contribute to the inability of CF lung tissues to control the inflammatory response or restore tissue homeostasis. The non-resolving hyper-inflammation in CF lungs is attributed to an impairment of several signaling pathways associated with resolution of the inflammatory response, including the heme oxygenase-1/carbon monoxide (HO-1/CO) pathway. HO-1 is an enzyme that degrades heme groups, leading to the production of potent antioxidant, anti-inflammatory, and bactericidal mediators, such as biliverdin, bilirubin, and CO. This pathway is fundamental to re-establishing cellular homeostasis in response to various insults, such as oxidative stress and infection. Monocytes/MΦs rely on abundant induction of the HO-1/CO pathway for a controlled immune response and for potent bactericidal activity. Here, we discuss studies showing that blunted HO-1 activation in CF-affected cells contributes to hyper-inflammation and defective host defense against bacteria. We dissect potential cellular mechanisms that may lead to decreased HO-1 induction in CF cells. We review literature suggesting that induction of HO-1 may be beneficial for the treatment of CF lung disease. Finally, we discuss recent studies highlighting how endogenous HO-1 can be induced by administration of controlled doses of CO to reduce lung hyper-inflammation, oxidative stress, bacterial infection, and dysfunctional ion transport, which are all hallmarks of CF lung disease.

Indexed as

carbon monoxide (CO)CO-releasing moleculescystic fibrosis (CF)heme oxygenase-1 (HO-1)lung inflammationmonocyte/macrophages

Identifiers

PMID32760278
PMCPMC7372134
OpenAlexW3043727069

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.