ArticleAmerican journal of physiology. Cell physiology2018
Cigarette smoke-induced autophagy impairment accelerates lung aging, COPD-emphysema exacerbations and pathogenesis.
Article in American journal of physiology. Cell physiology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 198 papers, 3 of them syntheses that pooled it.
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Who cites it
198 citing papers in PubMed, 3 syntheses or guidelines pooled it, 334 citations in OpenAlex.
- Revealing VNN1: An Emerging and Promising Target for Inflammation and Redox Balance.Immunity, inflammation and disease · 2025Pooled it
- p38 MAPK signaling in chronic obstructive pulmonary disease pathogenesis and inhibitor therapeutics.Cell communication and signaling : CCS · 2023Pooled it
- The interplay between oxidative stress and autophagy in chronic obstructive pulmonary disease.Frontiers in physiology · 2022Pooled it
- Oxidative Stress and Inflammatory Cytokines as Drivers of Cardiac Remodeling in COPD Patients.Antioxidants (Basel, Switzerland) · 2026Article
- Resveratrol Inhibits Macrophage Glucose Metabolism Reprogramming and Inflammatory Activation to Delay COPD Progression Through the TLR4/HK2 Pathway.Journal of cellular physiology · 2026Article
- Frailty and COPD: a bidirectional relationship in the context of systemic and accelerated ageing.European respiratory review : an official journal of the European Respiratory Society · 2026Review
- Autophagy as a Redox Rheostat Linking Cigarette Smoke, Electronic Cigarettes, and Nicotine Exposure to Lung Development, Disease, and Interorgan Communication.Comprehensive physiology · 2026Review
- Impact of emphysema on biomarkers in hospitalized COPD patients with community-acquired pneumonia: a retrospective study.BMC pulmonary medicine · 2026Article
- FOXD2-AS1/miR-185-5p/CDC42 axis in chronic obstructive pulmonary disease: clinical significance and mechanistic insights.Journal of inflammation (London, England) · 2026Article
- Hydrogen sulfide attenuates oxidative stress-induced cellular senescence via the Sirt3/SOD2 signaling pathway in chronic obstructive pulmonary disease.Chinese medical journal · 2026Article
- Interferon regulatory factor 5 involves the pathogenesis of emphysema through NLRP3 and Ly6C expressing cells.Experimental & molecular medicine · 2026Article
- <p>Cigarette smoke combined withMolecular medicine reports · 2026Article
- Oxidative stress-associated genes TPPP3 and VEGFA in COPD revealed by bulk and single-cell sequencing analysis.Scientific reports · 2026Article
- Scutellarein fromPharmaceuticals (Basel, Switzerland) · 2026Article
- Safety and efficacy of CT-guided percutaneous microwave ablation for stage I non-small cell lung cancer combined with moderate-to-severe pulmonary dysfunction.Frontiers in oncology · 2026Article
- β2-Microglobulin Induces Mitochondrial Dysfunction Accompanied by Bronchial Epithelial Cell Senescence.International journal of chronic obstructive pulmonary disease · 2026Article
- Mitophagy in kidney and lung epithelial cells: molecular mechanisms, crosstalk, and therapeutic interventions.Frontiers in physiology · 2026Review
- The mechanisms of energy balance between oxidative phosphorylation and glycolysis in human ovarian granulosa cells.Frontiers in physiology · 2026Article
- House dust mite-induced autophagy dysregulation and apoptosis in bronchial epithelial injury in asthma.Frontiers in pediatrics · 2026Article
- Cigarette smoke-induced circFOXO3 upregulation enhances autophagy-regulated senescence of type II alveolar cells through interacting with E2F1.Tobacco induced diseases · 2026Article
138 more citing papers are in PubMed but not listed here.
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Cigarette-smoke (CS) exposure and aging are the leading causes of chronic obstructive pulmonary disease (COPD)-emphysema development, although the molecular mechanism that mediates disease pathogenesis remains poorly understood. Our objective was to investigate the impact of CS exposure and aging on autophagy and the pathophysiological changes associated with lung aging (senescence) and emphysema progression. Beas2b cells, C57BL/6 mice, and human (GOLD 0-IV) lung tissues were used to determine the central mechanism involved in CS/age-related COPD-emphysema pathogenesis. Beas2b cells and murine lungs exposed to cigarette smoke extract (CSE)/CS showed a significant ( P < 0.05) accumulation of poly-ubiquitinated proteins and impaired autophagy marker, p62, in aggresome bodies. Moreover, treatment with the autophagy-inducing antioxidant drug cysteamine significantly ( P < 0.001) decreased CSE/CS-induced aggresome bodies. We also found a significant ( P < 0.001) increase in levels of aggresome bodies in the lungs of smokers and COPD subjects in comparison to nonsmoker controls. Furthermore, the presence and levels of aggresome bodies statistically correlated with severity of emphysema and alveolar senescence. In addition to CS exposure, lungs from old mice also showed accumulation of aggresome bodies, suggesting this as a common mechanism to initiate cellular senescence and emphysema. Additionally, Beas2b cells and murine lungs exposed to CSE/CS showed cellular apoptosis and senescence, which were both controlled by cysteamine treatment. In parallel, we evaluated the impact of CS on pulmonary exacerbation, using mice exposed to CS and/or infected with Pseudomonas aeruginosa ( Pa), and confirmed cysteamine's potential as an autophagy-inducing antibacterial drug, based on its ability to control CS-induced pulmonary exacerbation ( Pa-bacterial counts) and resulting inflammation. CS induced autophagy impairment accelerates lung aging and COPD-emphysema exacerbations and pathogenesis.
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Registered trials
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