ArticleRespiratory research2013
Prolonged cigarette smoke exposure alters mitochondrial structure and function in airway epithelial cells.
Article in Respiratory research, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 184 papers, 1 of them a synthesis that pooled it.
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Who cites it
184 citing papers in PubMed, 1 synthesis or guideline pooled it, 303 citations in OpenAlex.
- The interplay between oxidative stress and autophagy in chronic obstructive pulmonary disease.Frontiers in physiology · 2022Pooled it
- Fuelling repair: metabolic regulation of alveolar type 2 cell fate in lung regeneration and disease.Disease models & mechanisms · 2026Review
- Liquid tobacco-induced optic neuropathy in the tribal population of Northeast India.Indian journal of ophthalmology · 2026Article
- Adenine nucleotide translocase 2 (ANT2) deficiency reprograms ferroptosis in alveolar progenitor cells to promote emphysema.bioRxiv : the preprint server for biology · 2026Article
- Fueling the fire: metabolic dysfunction and senescence as drivers of lung aging and disease.Physiological reviews · 2026Review
- PDCD5 Contributes to Airway Epithelial Cell Damage via Mitochondrial Pathway and Participates in COPD Pathogenesis.The Kaohsiung journal of medical sciences · 2026Article
- A chronic whole cigarette smoke extract model reveals redox-mitochondrial adaptation in human lung epithelial and organoid models.Experimental & molecular medicine · 2026Article
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- Nicotine-induced mitophagy in bronchial epithelial cells and MYST1 downregulation in cigarette smoke-exposed lungs: potential mechanisms of COPD progression.Molecular biology reports · 2026Article
- Heat-Not-Burn Tobacco Aerosols Induce Immune Dysregulation and Barrier Disruption Comparable to Conventional Cigarettes.Allergy · 2026Article
- Kidney Dysfunction, Biochemical Changes, DNA Alteration, and MAPKs Regulation Following Chronic Exposure to Regular and Occasional Hookah Smoke in Mice.Oxidative medicine and cellular longevity · 2026Article
- β2-Microglobulin Induces Mitochondrial Dysfunction Accompanied by Bronchial Epithelial Cell Senescence.International journal of chronic obstructive pulmonary disease · 2026Article
- Muscle-lung crosstalk in COPD: how exercise training modulates protein metabolism and inflammation in experimental COPD models.Frontiers in immunology · 2026Review
- PRKN Ser131 phosphorylation promotes cigarette smoke-induced mitophagy impairment and epithelial cell senescence via MKK3/p38 MAPK activation: An in vitro and in vivo study.Tobacco induced diseases · 2026Article
- Mitochondrial stress response in lung cells triggered by the inhaled nanoplastics.Archives of toxicology · 2026Review
- GNPAT/USP30 Stabilizes DRP1 Protein to Promote Mitochondrial Fission and Functional Damage in COPD Progression.The Kaohsiung journal of medical sciences · 2025Article
- Emphysema Detection in Smokers: Diffusing Capacity for Nitric Oxide Beats Diffusing Capacity of Carbon Monoxide-Based Models.Chronic obstructive pulmonary diseases (Miami, Fla.) · 2025Article
- Particulate matter air pollution: effects on the respiratory system.The Journal of clinical investigation · 2025Review
- Lower Respiratory Tract Microbiome Signatures of Health and Lung Cancer Across Different Smoking Statuses.Cancers · 2025Article
124 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
14 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundCigarette smoking is the major risk factor for COPD, leading to chronic airway inflammation. We hypothesized that cigarette smoke induces structural and functional changes of airway epithelial mitochondria, with important implications for lung inflammation and COPD pathogenesis.
methodsWe studied changes in mitochondrial morphology and in expression of markers for mitochondrial capacity, damage/biogenesis and fission/fusion in the human bronchial epithelial cell line BEAS-2B upon 6-months from ex-smoking COPD GOLD stage IV patients to age-matched smoking and never-smoking controls.
resultsWe observed that long-term CSE exposure induces robust changes in mitochondrial structure, including fragmentation, branching and quantity of cristae. The majority of these changes were persistent upon CSE depletion. Furthermore, long-term CSE exposure significantly increased the expression of specific fission/fusion markers (Fis1, Mfn1, Mfn2, Drp1 and Opa1), oxidative phosphorylation (OXPHOS) proteins (Complex II, III and V), and oxidative stress (Mn-SOD) markers. These changes were accompanied by increased levels of the pro-inflammatory mediators IL-6, IL-8, and IL-1β. Importantly, COPD primary bronchial epithelial cells (PBECs) displayed similar changes in mitochondrial morphology as observed in long-term CSE-exposure BEAS-2B cells. Moreover, expression of specific OXPHOS proteins was higher in PBECs from COPD patients than control smokers, as was the expression of mitochondrial stress marker PINK1.
conclusionThe observed mitochondrial changes in COPD epithelium are potentially the consequence of long-term exposure to cigarette smoke, leading to impaired mitochondrial function and may play a role in the pathogenesis of COPD.
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Registered trials
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