ReviewAntioxidants & redox signaling2008
Deacetylases and NF-kappaB in redox regulation of cigarette smoke-induced lung inflammation: epigenetics in pathogenesis of COPD.
Review in Antioxidants & redox signaling, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 68 papers.
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.
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.
Who cites it
68 citing papers in PubMed, 155 citations in OpenAlex.
- Application of 18Journal of enzyme inhibition and medicinal chemistry · 2026Article
- Formononetin Alleviates Cigarette Smoke Extract-Induced Lung Injury in Mice with Gut Microbiota and Taurine/SLC6A6/NF-κB Modulation.Molecules (Basel, Switzerland) · 2026Article
- Emerging role of SIRT1 in asthma and COPD from molecular mechanisms to translational therapy.iScience · 2026Review
- Association of C-Reactive Protein-Triglyceride Glucose Index With Chronic Obstructive Pulmonary Disease: Results From the NHANES and CHARLS Cohorts.Mediators of inflammation · 2026Article
- Exercise and Epigenetic Regulation in COPD: Current Evidence and Potential Mechanistic Pathways.International journal of molecular sciences · 2025Review
- Unveiling the protective efficacy of rutin against High-Sucrose Diet-induced oxidative stress, biochemical alterations, and organismal hazards inToxicology research · 2025Article
- Histone Deacetylases (HDACs) Roles in Inflammation-mediated Diseases; Current Knowledge.Cell biochemistry and biophysics · 2025Review
- Review
- From metabolic alterations to chronic inflammation: mechanisms and immunoregulation of metabolic reprogramming in COPD.Frontiers in immunology · 2025Review
- Beneficial Effects ofNutrients · 2024Review
- Zinc-Dependent Histone Deacetylases in Lung Endothelial Pathobiology.Biomolecules · 2024Review
- Glucocorticoid-induced activation of NOX/ROS/NF-κB signaling in MSCs contributes to the development of GONFH.Apoptosis : an international journal on programmed cell death · 2023Article
- Endothelin-1 induces connective tissue growth factor expression in human lung fibroblasts by disrupting HDAC2/Sin3A/MeCP2 corepressor complex.Journal of biomedical science · 2023Article
- Modulation of Alveolar Macrophage Activity by Eugenol Attenuates Cigarette-Smoke-Induced Acute Lung Injury in Mice.Antioxidants (Basel, Switzerland) · 2023Article
- COPD Patients Exhibit Distinct Gene Expression, Accelerated Cellular Aging, and Bias to M2 Macrophages.International journal of molecular sciences · 2023Article
- Mechanisms of lung damage in tuberculosis: implications for chronic obstructive pulmonary disease.Frontiers in cellular and infection microbiology · 2023Review
- Mutagenic damage among bronchiectasis patients attending in the pulmonology sector of a hospital in southern Brazil.Revista da Associacao Medica Brasileira (1992) · 2022Article
- Prohibitin Protects Pulmonary Microvascular Endothelial Cells Against Cigarette Smoke Extract-Induced Cell Apoptosis and Inflammation.International journal of chronic obstructive pulmonary disease · 2022Article
- New Insight in HDACs: Potential Therapeutic Targets for the Treatment of Atherosclerosis.Frontiers in pharmacology · 2022Review
- Epigenetic Alterations under Oxidative Stress in Stem Cells.Oxidative medicine and cellular longevity · 2022Review
8 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Oxidative stress has been implicated in the pathogenesis of several inflammatory lung disorders including chronic obstructive pulmonary disease (COPD), due to its effect on pro-inflammatory gene transcription. Cigarette smoke-mediated oxidative stress activates NF-kappaB-dependent transcription of pro-inflammatory mediators either through activation of inhibitor kappaB-alpha kinase (IKK) and/or the enhanced recruitment and activation of transcriptional co-activators. Enhanced NF-kappaB-co-activator complex formation results in targeted increase in chromatin modifications, such as histone acetylation leading to inflammatory gene transcription. NF-kappaB-dependent gene expression, at least in part, is regulated by changes in deacetylases such as histone deacetylases (HDACs) and sirtuins. Cigarette smoke and oxidants also alter the activity of HDACs and sirtuins by post-translational modifications by protein carbonylation and nitration, and in doing so further induce gene expression of pro-inflammatory mediators by chromatin modifications. In addition, cigarette smoke/oxidants can reduce glucocorticoid sensitivity by attenuating HDAC2 activity and expression, which may account for the glucocorticoid insensitivity in patients with COPD. Understanding the mechanisms of NF-kappaB regulation, and the balance between histone acetylation and deacetylation may lead to the development of novel therapies based on the pharmacological manipulation of IKK and deacetylases in lung inflammation and injury.
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Registered trials
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.