Evidence map›Paper›PMID 29118026›Full record

ReviewAmerican journal of physiology. Cell physiology2018

Carbon monoxide in lung cell physiology and disease.

Stefan W Ryter, Kevin C Ma, Augustine M K Choi

Open access · bronzeAbstract readReview
In one paragraph

Review in American journal of physiology. Cell physiology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 71 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
71citing papers in PubMed, 1 pooled it
2.8field-weighted citation impact, top 9% 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

71 citing papers in PubMed, 1 synthesis or guideline pooled it, 130 citations in OpenAlex.

  1. Pooled it
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  17. The role of gasotransmitters in Parkinson's disease: Interplay of nitric oxide, carbon monoxide, and hydrogen sulfide.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2025
    Review
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11 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

3 authors at 1 institution in 1 country.

Stefan W RyterDivision of Pulmonary and Critical Care Medicine, Joan and Sanford I. Weill Department of Medicine, Weill Cornell Medical College , New York, New York.
Kevin C MaDivision of Pulmonary and Critical Care Medicine, Joan and Sanford I. Weill Department of Medicine, Weill Cornell Medical College , New York, New York.
Augustine M K ChoiDivision of Pulmonary and Critical Care Medicine, Joan and Sanford I. Weill Department of Medicine, Weill Cornell Medical College , New York, New York.
Cornell University · US

Funding

Mesenchymal Stromal Cell Conditioning by Carbon MonoxideP01HL108801 · NHLBI · BRIGHAM AND WOMEN'S HOSPITAL · PI CHOI, AUGUSTINE M · 2011 to 2015
$13.8M
The Role of HEME Oxygenase in Hyperoxic Lung InjuryR01HL055330 · NHLBI · YALE UNIVERSITY · PI CHOI, AUGUSTINE M, CHOI, MARY E · 1998 to 2021
$6.6M
HEME OXYGENASE 1--LUNG VASCULAR CELL HYPOXIC RESPONSER01HL060234 · NHLBI · YALE UNIVERSITY · PI CHOI, AUGUSTINE M, CHOI, MARY E · 1999 to 2017
$5.8M
Heme oxygenase-1: Regulation and Function in CaveolaeR01HL079904 · NHLBI · WEILL MEDICAL COLL OF CORNELL UNIV · PI CHOI, MARY E · 2005 to 2014
$2.9M
NHLBI NIH HHS P01 HL108801NHLBI NIH HHS R01 HL055330NHLBI NIH HHS R01 HL060234NHLBI NIH HHS R01 HL079904
6 · The paper itself

Abstract

Carbon monoxide (CO) is an endogenously produced gas that has gained recognition as a biological signal transduction effector with properties similar, but not identical, to that of nitric oxide (NO). CO, which binds primarily to heme iron, may activate the hemoprotein guanylate cyclase, although with lower potency than NO. Furthermore, CO can modulate the activities of several cellular signaling molecules such as p38 MAPK, ERK1/2, JNK, Akt, NF-κB, and others. Emerging studies suggest that mitochondria, the energy-generating organelle of cells, represent a key target of CO action in eukaryotes. Dose-dependent modulation of mitochondrial function by CO can result in alteration of mitochondrial membrane potential, mitochondrial reactive oxygen species production, release of proapoptotic and proinflammatory mediators, as well as the inhibition of respiration at high concentration. CO, through modulation of signaling pathways, can impact key biological processes including autophagy, mitochondrial biogenesis, programmed cell death (apoptosis), cellular proliferation, inflammation, and innate immune responses. Inhaled CO is widely known as an inhalation hazard due to its rapid complexation with hemoglobin, resulting in impaired oxygen delivery to tissues and hypoxemia. Despite systemic and cellular toxicity at high concentrations, CO has demonstrated cyto- and tissue-protective effects at low concentration in animal models of organ injury and disease. These include models of acute lung injury (e.g., hyperoxia, hypoxia, ischemia-reperfusion, mechanical ventilation, bleomycin) and sepsis. The success of CO as a candidate therapeutic in preclinical models suggests potential clinical application in inflammatory and proliferative disorders, which is currently under evaluation in clinical trials.

Indexed as

AnimalsCarbon MonoxideDose-Response Relationship, DrugHumansLungLung DiseasesMitochondriaSignal TransductionCarbon Monoxidecarbon monoxidecell deathcell signalinginflammationlung diseasemitochondriareactive oxygen speciessepsis

Identifiers

PMID29118026
PMCPMC5866434
OpenAlexW2767358501

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.