Evidence map›Paper›PMID 21296096›Full record

ReviewToxicology and applied pharmacology2011

Current concepts on oxidative/carbonyl stress, inflammation and epigenetics in pathogenesis of chronic obstructive pulmonary disease.

Hongwei Yao, Irfan Rahman

Open access · greenAbstract readReview
In one paragraph

Review in Toxicology and applied pharmacology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 114 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
114citing papers in PubMed, 1 pooled it
21.9field-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

114 citing papers in PubMed, 1 synthesis or guideline pooled it, 245 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Review
  4. Article
  5. Review
  6. Involvement of oxidative stress in post-acute sequelae of COVID-19: clinical implications.Redox report : communications in free radical research · 2025
    Article
  7. Article
  8. Article
  9. Article
  10. Review
  11. Article
  12. Review
  13. Review
  14. Dysregulation of miR-103a Mediates Cigarette Smoking-induced Lipid-laden Macrophage Formation.American journal of respiratory cell and molecular biology · 2022
    Article
  15. Article
  16. Review
  17. Article
  18. Review
  19. Article
  20. Review

54 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

2 authors at 1 institution in 1 country.

Hongwei YaoDepartment of Environmental Medicine, Lung Biology and Disease Program, University of Rochester Medical Center, Rochester, NY 1464, USA.
Irfan Rahman
University of Rochester Medical Center · US

Funding

VISUAL INDICES OF NEUROTOXICITYP30ES001247 · NIEHS · UNIVERSITY OF ROCHESTER · PI Martha Susiarjo · 1985 to 2026
$42.8M
MECHANISMS OF CIGARETTE SMOKE-INDUCED LUNG CELLULAR SENESCENCER01HL085613 · NHLBI · UNIVERSITY OF ROCHESTER · PI RAHMAN, IRFAN · 2007 to 2017
$4.0M
CIRCADIAN-COUPLED CELLULAR AND LUNG FUNCTION IN COPDR01HL097751 · NHLBI · UNIVERSITY OF ROCHESTER · PI RAHMAN, IRFAN · 2009 to 2012
$1.9M
ROLE OF SIRTUIN IN CIGARETTE SMOKE-INDUCED LUNG INFLAMMATION AND INJURYR01HL092842 · NHLBI · UNIVERSITY OF ROCHESTER · PI RAHMAN, IRFAN · 2010 to 2013
$1.5M
NHLBI NIH HHS 1R01HL085613NHLBI NIH HHS 1R01HL092842NHLBI NIH HHS 1R01HL097751NHLBI NIH HHS R01 HL085613NHLBI NIH HHS R01 HL092842NHLBI NIH HHS R01 HL097751NIEHS NIH HHS ES01247NIEHS NIH HHS P30 ES001247
6 · The paper itself

Abstract

Chronic obstructive pulmonary disease (COPD) is a global health problem. The current therapies for COPD are poorly effective and the mainstays of pharmacotherapy are bronchodilators. A better understanding of the pathobiology of COPD is critical for the development of novel therapies. In the present review, we have discussed the roles of oxidative/aldehyde stress, inflammation/immunity, and chromatin remodeling in the pathogenesis of COPD. An imbalance of oxidants/antioxidants caused by cigarette smoke and other pollutants/biomass fuels plays an important role in the pathogenesis of COPD by regulating redox-sensitive transcription factors (e.g., NF-κB), autophagy and unfolded protein response leading to chronic lung inflammatory response. Cigarette smoke also activates canonical/alternative NF-κB pathways and their upstream kinases leading to sustained inflammatory response in lungs. Recently, epigenetic regulation has been shown to be critical for the development of COPD because the expression/activity of enzymes that regulate these epigenetic modifications have been reported to be abnormal in airways of COPD patients. Hence, the significant advances made in understanding the pathophysiology of COPD as described herein will identify novel therapeutic targets for intervention in COPD.

Indexed as

AnimalsAntioxidantsEpigenesis, GeneticHumansInflammationOxidative StressProtein CarbonylationPulmonary Disease, Chronic ObstructiveSignal TransductionSmokingAntioxidants

Identifiers

PMID21296096
PMCPMC3107364
OpenAlexW2008636933

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.