Evidence map›Paper›PMID 31486024›Full record

ReviewArchives of pharmacal research2020

Mitochondrial biology in airway pathogenesis and the role of NRF2.

Hye-Youn Cho, Steven R Kleeberger

Open access · greenAbstract readReview
In one paragraph

Review in Archives of pharmacal research, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing 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

26 citing papers in PubMed, 37 citations in OpenAlex.

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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

2 authors at 1 institution in 1 country.

Hye-Youn ChoImmunity, Inflammation, and Disease Laboratory, National Institute of Environmental Health Sciences, 111 TW Alexander Dr., Research Triangle Park, NC, 27709, USA. cho2@niehs.nih.gov.ORCID http://orcid.org/0000-0002-8671-8544
Steven R KleebergerImmunity, Inflammation, and Disease Laboratory, National Institute of Environmental Health Sciences, 111 TW Alexander Dr., Research Triangle Park, NC, 27709, USA.
National Institute of Environmental Health Sciences · US

Funding

The Role Of Nrf2 In Susceptibility To Hyperoxic Lung InjuryZIAES100513 · NIEHS · NATIONAL INSTITUTE OF ENVIRONMENTAL HEALTH SCIENCES · PI KLEEBERGER, STEVEN R · 2009 to 2021
$11.5M
The Role Of Innate Immunity Genes In Viral Infection and Disease ProgressionZIAES100557 · NIEHS · NATIONAL INSTITUTE OF ENVIRONMENTAL HEALTH SCIENCES · PI KLEEBERGER, STEVEN R · 2009 to 2021
$10.9M
The Role Of Nrf2 In Susceptibility To Hyperoxic Lung InjuryZ01ES100513 · NIEHS · NATIONAL INSTITUTE OF ENVIRONMENTAL HEALTH SCIENCES · PI KLEEBERGER, STEVEN R · 2002 to 2008
$890k
Intramural NIH HHS Z01 ES100513
6 · The paper itself

Abstract

A constant improvement in understanding of mitochondrial biology has provided new insights into mitochondrial dysfunction in human disease pathogenesis. Impaired mitochondrial dynamics caused by various stressors are characterized by structural abnormalities and leakage, compromised turnover, and reactive oxygen species overproduction in mitochondria as well as increased mitochondrial DNA mutation frequency, which leads to modified energy production and mitochondria-derived cell signaling. The mitochondrial dysfunction in airway epithelial, smooth muscle, and endothelial cells has been implicated in diseases including chronic obstructive lung diseases and acute lung injury. Increasing evidence indicates that the NRF2-antioxidant response element (ARE) pathway not only enhances redox defense but also facilitates mitochondrial homeostasis and bioenergetics. Identification of functional or potential AREs further supports the role for Nrf2 in mitochondrial dysfunction-associated airway disorders. While clinical reports indicate mixed efficacy, NRF2 agonists acting on respiratory mitochondrial dynamics are potentially beneficial. In lung cancer, growth advantage provided by sustained NRF2 activation is suggested to be through increased cellular antioxidant defense as well as mitochondria reinforcement and metabolic reprogramming to the preferred pathways to meet the increased energy demands of uncontrolled cell proliferation. Further studies are warranted to better understand NRF2 regulation of mitochondrial functions as therapeutic targets in airway disorders.

Indexed as

AnimalsAntioxidant Response ElementsHumansMitochondriaNF-E2-Related Factor 2Oxidation-ReductionRespiration DisordersNF-E2-Related Factor 2Antioxidant response elementLungMetabolismMitochondriaNRF2Sulforaphane

Identifiers

PMID31486024
PMCPMC7054182
OpenAlexW2971907632

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.