Evidence map›Paper›PMID 22978694›Full record

ReviewAntioxidants & redox signaling2013

Oxidative stress and chromatin remodeling in chronic obstructive pulmonary disease and smoking-related diseases.

Isaac K Sundar, Hongwei Yao, Irfan Rahman

Open access · greenAbstract readReview
In one paragraph

Review in Antioxidants & redox signaling, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 91 papers.

0numbers the graph read from it
0cells of the map it votes in
91citing papers in PubMed
4.4field-weighted citation impact, top 5% 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

91 citing papers in PubMed, 187 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Review
  5. Review
  6. Article
  7. Review
  8. Article
  9. Review
  10. Epigenetics and environmental health.Frontiers of medicine · 2024
    Review
  11. Article
  12. Effect of Adrenocorticotropic Hormone Stimulation on Ischemiamodified Albumin LevelsJournal of clinical research in pediatric endocrinology · 2024
    Article
  13. Article
  14. Article
  15. Article
  16. Review
  17. Article
  18. Article
  19. Article
  20. Effects of E-Cigarette Flavoring Chemicals on Human Macrophages and Bronchial Epithelial Cells.International journal of environmental research and public health · 2021
    Article

31 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 1 institution in 1 country.

Isaac K SundarDepartment of Environmental Medicine, Lung Biology and Disease Program, University of Rochester Medical Center, Rochester, New York 14642, USA.
Hongwei Yao
Irfan Rahman
University of Rochester Medical Center · US

Funding

VISUAL INDICES OF NEUROTOXICITYP30ES001247 · NIEHS · UNIVERSITY OF ROCHESTER · PI B Paige Lawrence · 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 1R01HL097751NIEHS NIH HHS P30-ES01247
6 · The paper itself

Abstract

significanceChronic obstructive pulmonary disease (COPD) is predominantly a tobacco smoke-triggered disease with features of chronic low-grade systemic inflammation and aging (inflammaging) of the lung associated with steroid resistance induced by cigarette smoke (CS)-mediated oxidative stress. Oxidative stress induces various kinase signaling pathways leading to chromatin modifications (histone acetylation/deacetylation and histone methylation/demethylation) in inflammation, senescence, and steroid resistance. RECENT ADVANCES: Histone mono-, di-, or tri-methylation at lysine residues result in either gene activation (H3K4, H3K36, and H3K79) or repression (H3K9, H3K27, and H3K20). Cross-talk occurs between various epigenetic marks on histones and DNA methylation. Both CS and oxidants alter histone acetylation/deacetylation and methylation/demethylation leading to enhanced proinflammatory gene expression. Chromatin modifications occur in lungs of patients with COPD. Histone deacetylase 2 (HDAC2) reduction (levels and activity) is associated with steroid resistance in response to oxidative stress. CRITICAL ISSUES: Histone modifications are associated with DNA damage/repair and epigenomic instability as well as premature lung aging, which have implications in the pathogenesis of COPD. HDAC2/SIRTUIN1 (SIRT1)-dependent chromatin modifications are associated with DNA damage-induced inflammation and senescence in response to CS-mediated oxidative stress. FUTURE DIRECTIONS: Understanding CS/oxidative stress-mediated chromatin modifications and the cross-talk between histone acetylation and methylation will demonstrate the involvement of epigenetic regulation of chromatin remodeling in inflammaging. This will lead to identification of novel epigenetic-based therapies against COPD and other smoking-related lung diseases. Pharmacological activation of HDAC2/SIRT1 or reversal of their oxidative post-translational modifications may offer therapies for treatment of COPD and CS-related diseases based on epigenetic histone modifications.

Indexed as

Chromatin Assembly and DisassemblyOxidative StressSmokingAcetylationDNA MethylationHistonesHumansMethylationOxidation-ReductionPhosphotransferasesPulmonary Disease, Chronic ObstructiveSignal TransductionHistonesPhosphotransferases

Identifiers

PMID22978694
PMCPMC3624634
OpenAlexW2105922101

What OpenQuestion holds

Textmetadata
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.