ArticleExperimental lung research2010
Peroxiredoxin 6 differentially regulates acute and chronic cigarette smoke–mediated lung inflammatory response and injury.
Article in Experimental lung research, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
What it found
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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.
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Who cites it
15 citing papers in PubMed, 43 citations in OpenAlex.
- Joint clinical and molecular subtyping of COPD with variational autoencoders.Nature communications · 2026Article
- Molecular Impact of Conventional and Electronic Cigarettes on Pulmonary Surfactant.International journal of molecular sciences · 2023Review
- Effect of PRDX6 gene polymorphism on susceptibility to chronic obstructive pulmonary disease in the Chinese Han population.The clinical respiratory journal · 2023Article
- Epithelial Ablation of Miro1/Rhot1 GTPase Augments Lung Inflammation by Cigarette Smoke.Pathophysiology : the official journal of the International Society for Pathophysiology · 2021Article
- The Roles of Peroxiredoxin 6 in Brain Diseases.Molecular neurobiology · 2021Review
- Lack of the peroxiredoxin 6 gene causes impaired spatial memory and abnormal synaptic plasticity.Molecular brain · 2021Article
- Targeted antioxidants as therapeutics for treatment of pneumonia in the elderly.Translational research : the journal of laboratory and clinical medicine · 2020Review
- Knockout Mouse Models for Peroxiredoxins.Antioxidants (Basel, Switzerland) · 2020Review
- Functional screening implicates miR-371-3p and peroxiredoxin 6 in reversible tolerance to cancer drugs.Nature communications · 2016Article
- Cigarette smoke induces distinct histone modifications in lung cells: implications for the pathogenesis of COPD and lung cancer.Journal of proteome research · 2014Article
- Risk assessment, disease prevention and personalised treatments in breast cancer: is clinically qualified integrative approach in the horizon?The EPMA journal · 2013Article
- Mouse Models of Oxidative Stress Indicate a Role for Modulating Healthy Aging.Journal of clinical & experimental pathology · 2012Article
- Strategies to decrease ongoing oxidant burden in chronic obstructive pulmonary disease.Expert review of clinical pharmacology · 2012Review
- Pharmacological antioxidant strategies as therapeutic interventions for COPD.Biochimica et biophysica acta · 2012Review
- Lung glutathione adaptive responses to cigarette smoke exposure.Respiratory research · 2011Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors at 4 institutions in 2 countries.
Funding
Abstract
Peroxiredoxin 6 (Prdx6) exerts its protective role through peroxidase activity against H₂O₂ and phospholipid hydroperoxides. We hypothesized that targeted disruption of Prdx6 would lead to enhanced susceptibility to cigarette smoke (CS)-mediated lung inflammation and/or emphysema in mouse lung. Prdx6 null (Prdx6⁻/⁻mice exposed to acute CS showed no significant increase of inflammatory cell influx or any alterations in lung levels of proinflammatory cytokines compared to wild-type (WT) mice. Lung levels of antioxidant enzymes were significantly increased in acute CS-exposed Prdx6⁻/⁻ compared to WT mice. Overexpressing (Prdx6⁻/⁻) mice exposed to acute CS showed significant decrease in lung antioxidant enzymes associated with increased inflammatory response compared to CS-exposed WT mice or air-exposed Prdx6⁻/⁻ mice. However, chronic 6 months of CS exposure resulted in increased lung inflammatory response, mean linear intercept (Lm), and alteration in lung mechanical properties in Prdx6⁻/⁻ when compared to WT mice exposed to CS. These data show that targeted disruption of Prdx6 does not lead to increased lung inflammatory response but is associated with increased antioxidants, suggesting a critical role of lung Prdx6 and several compensatory mechanisms during acute CS-induced adaptive response, whereas this protection is lost in chronic CS exposure leading to emphysema.
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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.