ArticleInternational journal of molecular sciences2022
Smoking Cessation in Mice Does Not Switch off Persistent Lung Inflammation and Does Not Restore the Expression of HDAC2 and SIRT1.
Article in International journal of molecular sciences, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers, 1 of them a synthesis that pooled it.
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The trial behind it
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Who cites it
10 citing papers in PubMed, 1 synthesis or guideline pooled it, 13 citations in OpenAlex.
- Effects of smoking cessation on individuals with COPD: a systematic review and meta-analysis.Frontiers in public health · 2024Pooled it
- Prevalence of PRISm and COPD and associated factors in a university medical centre spirometry unit: a cross-sectional analysis.BMJ open · 2026Article
- Integrative Genomic and AI Approaches to Lung Cancer and Implications for Disease Prevention in Former Smokers.International journal of molecular sciences · 2026Review
- AMPK/SIRT1/PGC-1α Signaling Pathway: Molecular Mechanisms and Targeted Strategies From Energy Homeostasis Regulation to Disease Therapy.CNS neuroscience & therapeutics · 2025Review
- Identification of Novel Biomarkers Associated with Corticosteroid Resistance in Asthma by Bioinformatics Analysis and Experimental Validation.Journal of inflammation research · 2025Article
- Implications of DNA damage in chronic lung disease.Frontiers in cell and developmental biology · 2024Review
- Immunohistochemical Study of Airways Fibrous Remodeling in Smoking Mice.The journal of histochemistry and cytochemistry : official journal of the Histochemistry Society · 2023Article
- Advances in Molecular and Translational Medicine.International journal of molecular sciences · 2023Article
- Effects of Smoking on Outcomes of Anti-Vascular Endothelial Growth Factor Therapy in Patients with Diabetic Macular Edema: A Retrospective Case-Control Study.Middle East African journal of ophthalmologyArticle
- Modernisation of chronic respiratory disease management: The integration of wearable technology.Chronic respiratory diseaseReview
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Once COPD is established, pulmonary lesions can only progress and smoking cessation by itself is not sufficient to switch off persistent lung inflammation. Similarly, in former-smoker mice, neutrophil inflammation persists and lung lesions undergo progressive deterioration. The molecular mechanisms underlying disease progression and the inefficiency of smoking cessation in quenching neutrophilic inflammation were studied in male C57 Bl/6 mice after 6 months of rest from smoking cessation. As compared with the mice that continued to smoke, the former-smoker mice showed reduced expression of histone deacetylases HDAC2 and SIRT1 and marked expression of p-p38 MAPK and p-Ser10. All these factors are involved in corticosteroid insensitivity and in perpetuating inflammation. Former-smoker mice do show persistent lung neutrophilic influx and a high number of macrophages which account for the intense staining in the alveolar structures of neutrophil elastase and MMP-9 (capable of destroying lung scaffolding) and 8-OHdG (marker of oxidative stress). "Alarmins" released from necrotic cells together with these factors can sustain and perpetuate inflammation after smoking cessation. Several factors and mechanisms all together are involved in sustaining and perpetuating inflammation in former-smoker mice. This study suggests that a better control of COPD in humans may be achieved by precise targeting of the various molecular mechanisms associated with different phenotypes of disease by using a cocktail of drug active toward specific molecules.
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Registered trials
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