Evidence map›Paper›PMID 23219955›Full record

ReviewBiochimica et biophysica acta2013

Oxidative stress and pulmonary fibrosis.

Paul Cheresh, Seok-Jo Kim, Sandhya Tulasiram, David W Kamp

Abstract readReview
In one paragraph

Review in Biochimica et biophysica acta, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 266 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
266citing papers in PubMed, 2 pooled it
12.2field-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

266 citing papers in PubMed, 2 syntheses or guidelines pooled it, 533 citations in OpenAlex.

  1. Pooled it
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  9. Synthesis and crystal structure analysis of (3aActa crystallographica. Section E, Crystallographic communications · 2026
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  15. Synthesis, crystal structure and Hirshfeld surface analysis of (3aActa crystallographica. Section E, Crystallographic communications · 2026
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206 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

4 authors at 2 institutions in 1 country.

Paul ChereshDepartment of Medicine, Northwestern University Feinberg School of Medicine and Jesse Brown VA Medical Center, USA.
Seok-Jo Kim
Sandhya Tulasiram
David W Kamp
Jesse Brown VA Medical Center · USNorthwestern University · US

Funding

Tumor Environment and Metastasis (TEAM) Research ProgramP30CA060553 · NCI · NORTHWESTERN UNIVERSITY AT CHICAGO · PI Daniela E Matei · 1993 to 2026
$153.9M
Mitigation of asbestos induced alveolar epithelial cell injuryR01ES020357 · NIEHS · NORTHWESTERN UNIVERSITY AT CHICAGO · PI KAMP, DAVID W · 2012 to 2016
$1.6M
Mechanisms of Asbestos-Induced Alveolar Epithelial Cell InjuryI01BX000786 · VA · JESSE BROWN VA MEDICAL CENTER · PI KAMP, DAVID W · 2012 to 2021
–
BLRD VA I01 BX000786NCI NIH HHS P30 CA060553NIEHS NIH HHS R01 ES020357
6 · The paper itself

Abstract

Oxidative stress is implicated as an important molecular mechanism underlying fibrosis in a variety of organs, including the lungs. However, the causal role of reactive oxygen species (ROS) released from environmental exposures and inflammatory/interstitial cells in mediating fibrosis as well as how best to target an imbalance in ROS production in patients with fibrosis is not firmly established. We focus on the role of ROS in pulmonary fibrosis and, where possible, highlight overlapping molecular pathways in other organs. The key origins of oxidative stress in pulmonary fibrosis (e.g. environmental toxins, mitochondria/NADPH oxidase of inflammatory and lung target cells, and depletion of antioxidant defenses) are reviewed. The role of alveolar epithelial cell (AEC) apoptosis by mitochondria- and p53-regulated death pathways is examined. We emphasize an emerging role for the endoplasmic reticulum (ER) in pulmonary fibrosis. After briefly summarizing how ROS trigger a DNA damage response, we concentrate on recent studies implicating a role for mitochondrial DNA (mtDNA) damage and repair mechanisms focusing on 8-oxoguanine DNA glycosylase (Ogg1) as well as crosstalk between ROS production, mtDNA damage, p53, Ogg1, and mitochondrial aconitase (ACO2). Finally, the association between ROS and TGF-β1-induced fibrosis is discussed. Novel insights into the molecular basis of ROS-induced pulmonary diseases and, in particular, lung epithelial cell death may promote the development of unique therapeutic targets for managing pulmonary fibrosis as well as fibrosis in other organs and tumors, and in aging; diseases for which effective management is lacking. This article is part of a Special Issue entitled: Fibrosis: Translation of basic research to human disease.

Indexed as

Oxidative StressPulmonary FibrosisAnimalsApoptosisDNA, MitochondrialHumansMitochondriaDNA, Mitochondrial

Identifiers

PMID23219955
PMCPMC3639303
OpenAlexW1968477506

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.