Evidence map›Paper›PMID 32818797›Full record

ReviewRedox biology2020

Complex interplay between autophagy and oxidative stress in the development of pulmonary disease.

Wojciech Ornatowski, Qing Lu, Manivannan Yegambaram, Alejandro E Garcia, Evgeny A Zemskov, Emin Maltepe, Jeffrey R Fineman, Ting Wang, Stephen M Black

Open access · goldAbstract readReview
In one paragraph

Review in Redox biology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 240 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
240citing papers in PubMed, 2 pooled it
26.6field-weighted citation impact, top 1% 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

240 citing papers in PubMed, 2 syntheses or guidelines pooled it, 436 citations in OpenAlex.

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180 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

9 authors at 2 institutions in 1 country.

Wojciech OrnatowskiDepartment of Medicine, The University of Arizona Health Sciences, Tucson, AZ, USA.
Qing LuDepartment of Medicine, The University of Arizona Health Sciences, Tucson, AZ, USA.
Manivannan YegambaramDepartment of Medicine, The University of Arizona Health Sciences, Tucson, AZ, USA.
Alejandro E GarciaDepartment of Medicine, The University of Arizona Health Sciences, Tucson, AZ, USA.
Evgeny A ZemskovDepartment of Medicine, The University of Arizona Health Sciences, Tucson, AZ, USA.
Emin MaltepeDepartment of Pediatrics, The University of California, San Francisco, San Francisco, CA, USA.
Jeffrey R FinemanDepartment of Pediatrics, The University of California, San Francisco, San Francisco, CA, USA; Cardiovascular Research Institute, University of California, San Francisco, San Francisco, CA, USA.
Ting WangDepartment of Internal Medicine, The University of Arizona Health Sciences, Phoenix, AZ, USA.
Stephen M BlackDepartment of Medicine, The University of Arizona Health Sciences, Tucson, AZ, USA. Electronic address: steveblack@email.arizona.edu.
University of Arizona · USUniversity of California, San Francisco · US

Funding

SOUTHWEST ENVIRONMENTAL HEALTH SCIENCES CENTERP30ES006694 · NIEHS · UNIVERSITY OF ARIZONA · PI DEAN BILLHEIMER · 1994 to 2026
$36.7M
TGF-ß-SOX18-Collagen metabolism in pulmonary vascular disease associated with CHDP01HL146369 · NHLBI · UNIVERSITY OF ARIZONA · PI Stephen M Black · 2020 to 2026
$18.7M
Protein Chemistry & Biophysics CoreP01HL134610 · NHLBI · UNIVERSITY OF ARIZONA · PI BLACK, STEPHEN M · 2018 to 2022
$11.6M
PERINATAL PULMONARY HYPERTENSION: DEVELOPMENT MEDIATORSR01HL061284 · NHLBI · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI FINEMAN, JEFFREY R · 1999 to 2016
$8.3M
PERINATAL REGULATION OF THE ENDOTHELIAL NOS GENER01HL060190 · NHLBI · UNIVERSITY OF MONTANA · PI Stephen M Black · 1998 to 2026
$7.1M
Perinatal NO signaling in congenital heart diseaseR01HL137282 · NHLBI · UNIVERSITY OF ARIZONA · PI BLACK, STEPHEN M, FINEMAN, JEFFREY R · 2017 to 2020
$2.7M
PKG Signaling and Sepsis Induced ALIR01HL142212 · NHLBI · UNIVERSITY OF ARIZONA · PI BLACK, STEPHEN M, ZEMSKOV, EVGENY A. · 2018 to 2021
$1.8M
NHLBI NIH HHS P01 HL134610NHLBI NIH HHS P01 HL146369NHLBI NIH HHS R01 HL060190NHLBI NIH HHS R01 HL061284NHLBI NIH HHS R01 HL137282NHLBI NIH HHS R01 HL142212NIEHS NIH HHS P30 ES006694
6 · The paper itself

Abstract

The autophagic pathway involves the encapsulation of substrates in double-membraned vesicles, which are subsequently delivered to the lysosome for enzymatic degradation and recycling of metabolic precursors. Autophagy is a major cellular defense against oxidative stress, or related conditions that cause accumulation of damaged proteins or organelles. Selective forms of autophagy can maintain organelle populations or remove aggregated proteins. Dysregulation of redox homeostasis under pathological conditions results in excessive generation of reactive oxygen species (ROS), leading to oxidative stress and the associated oxidative damage of cellular components. Accumulating evidence indicates that autophagy is necessary to maintain redox homeostasis. ROS activates autophagy, which facilitates cellular adaptation and diminishes oxidative damage by degrading and recycling intracellular damaged macromolecules and dysfunctional organelles. The cellular responses triggered by oxidative stress include the altered regulation of signaling pathways that culminate in the regulation of autophagy. Current research suggests a central role for autophagy as a mammalian oxidative stress response and its interrelationship to other stress defense systems. Altered autophagy phenotypes have been observed in lung diseases such as chronic obstructive lung disease, acute lung injury, cystic fibrosis, idiopathic pulmonary fibrosis, and pulmonary arterial hypertension, and asthma. Understanding the mechanisms by which ROS regulate autophagy will provide novel therapeutic targets for lung diseases. This review highlights our current understanding on the interplay between ROS and autophagy in the development of pulmonary disease.

Indexed as

AutophagyLung DiseasesAnimalsOxidation-ReductionOxidative StressReactive Oxygen SpeciesReactive Oxygen SpeciesAutophagyMitochondriaMitophagyOxidative stressPulmonary diseaseReactive oxygen species

Identifiers

PMID32818797
PMCPMC7451718
OpenAlexW3048520812

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.