Evidence map›Paper›PMID 23347351›Full record

ReviewAnnual review of pathology2013

Molecular basis of asbestos-induced lung disease.

Gang Liu, Paul Cheresh, David W Kamp

Open access · greenAbstract readReview
In one paragraph

Review in Annual review of pathology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 87 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
87citing papers in PubMed, 2 pooled it
15.2field-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

87 citing papers in PubMed, 2 syntheses or guidelines pooled it, 210 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Murine models of pulmonary fibrosis: mechanisms, limitations and translational insights.European respiratory review : an official journal of the European Respiratory Society · 2026
    Review
  4. Review
  5. Review
  6. Immunological mechanisms and therapeutic approaches in pulmonary fibrosis.European respiratory review : an official journal of the European Respiratory Society · 2026
    Review
  7. Article
  8. Article
  9. Article
  10. Review
  11. Review
  12. Environmental Causes of Idiopathic Pulmonary Fibrosis.International journal of molecular sciences · 2023
    Review
  13. Article
  14. HMGB1 released by mesothelial cells drives the development of asbestos-induced mesothelioma.Proceedings of the National Academy of Sciences of the United States of America · 2023
    Article
  15. Review
  16. Oxidative Stress and Lung Fibrosis: Towards an Adverse Outcome Pathway.International journal of molecular sciences · 2023
    Review
  17. Review
  18. Article
  19. Article
  20. Article

27 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 2 institutions in 2 countries.

Gang LiuClinical Research Center, Affiliated Hospital of Guangdong Medical College, Zhangjiang, China. docgangliu@hotmail.com
Paul Cheresh
David W Kamp
Northwestern University · USGuangdong Medical College · CN

Funding

Mitigation of asbestos induced alveolar epithelial cell injuryR01ES020357 · NIEHS · NORTHWESTERN UNIVERSITY AT CHICAGO · PI KAMP, DAVID W · 2012 to 2016
$1.6M
BLRD VA I01 BX000786NIEHS NIH HHS R01 ES020357NIEHS NIH HHS R01ES020357
6 · The paper itself

Abstract

Asbestos causes asbestosis and malignancies by molecular mechanisms that are not fully understood. The modes of action underlying asbestosis, lung cancer, and mesothelioma appear to differ depending on the fiber type, lung clearance, and genetics. After reviewing the key pathologic changes following asbestos exposure, we examine recently identified pathogenic pathways, with a focus on oxidative stress. Alveolar epithelial cell apoptosis, which is an important early event in asbestosis, is mediated by mitochondria- and p53-regulated death pathways and may be modulated by the endoplasmic reticulum. We review mitochondrial DNA (mtDNA)-damage and -repair mechanisms, focusing on 8-oxoguanine DNA glycosylase, as well as cross talk between reactive oxygen species production, mtDNA damage, p53, OGG1, and mitochondrial aconitase. These new insights into the molecular basis of asbestos-induced lung diseases may foster the development of novel therapeutic targets for managing degenerative diseases (e.g., asbestosis and idiopathic pulmonary fibrosis), tumors, and aging, for which effective management is lacking.

Indexed as

AnimalsApoptosisAsbestosAsbestosisDNA DamageDNA, MitochondrialHumansLung DiseasesLung NeoplasmsMesotheliomaOxidative StressReactive Oxygen SpeciesAsbestosDNA, MitochondrialReactive Oxygen Species

Identifiers

PMID23347351
PMCPMC3900296
OpenAlexW2114601629

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.