ReviewEuropean respiratory review : an official journal of the European Respiratory Society2017
Is mitochondrial dysfunction a driving mechanism linking COPD to nonsmall cell lung carcinoma?
Review in European respiratory review : an official journal of the European Respiratory Society, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
27 citing papers in PubMed, 53 citations in OpenAlex.
- Ylang Ylang Essential Oil in Malignant and Non-Malignant Cells: Comparative Mitophagy-Related Transcriptional Responses.Pharmaceuticals (Basel, Switzerland) · 2026Article
- Machine learning-driven identification of shared and disease-specific mitochondria-related genes in COPD, NSCLC, and NSCLC with COPD.iScience · 2026Article
- Review
- Integrating Multi-Omics Data to Uncover Causal Links Between Mitochondria-Related Genes and Chronic Obstructive Pulmonary Disease: A Mendelian Randomization Study.International journal of chronic obstructive pulmonary disease · 2026Article
- A comprehensive analysis of the relationship between inflammasomes and autophagy in human tumors: Recent developments.Journal of cell communication and signaling · 2025Review
- Inflammation in cancer: therapeutic opportunities from new insights.Molecular cancer · 2025Review
- Drp1: Focus on Diseases Triggered by the Mitochondrial Pathway.Cell biochemistry and biophysics · 2024Review
- Review
- The role of extracellular vesicles in COPD and potential clinical value.Respiratory research · 2024Review
- Insights into the role of mitophagy in lung cancer: current evidence and perspectives.Frontiers in pharmacology · 2024Review
- Pre-clinical lung squamous cell carcinoma mouse models to identify novel biomarkers and therapeutic interventions.Frontiers in oncology · 2023Review
- Article
- Altered expression of ACOX2 in non-small cell lung cancer.BMC pulmonary medicine · 2022Article
- Cellular Senescence in Aging Lungs and Diseases.Cells · 2022Review
- Recent progress in the use of mitochondrial membrane permeability transition pore in mitochondrial dysfunction-related disease therapies.Molecular and cellular biochemistry · 2021Review
- Mitochondrial dysfunction in lung ageing and disease.European respiratory review : an official journal of the European Respiratory Society · 2020Review
- Crosstalks between inflammasome and autophagy in cancer.Journal of hematology & oncology · 2020Review
- Compression-induced senescence of nucleus pulposus cells by promoting mitophagy activation via the PINK1/PARKIN pathway.Journal of cellular and molecular medicine · 2020Article
- TNFRSF12A and CD38 Contribute to a Vicious Circle for Chronic Obstructive Pulmonary Disease by Engaging Senescence Pathways.Frontiers in cell and developmental biology · 2020Article
- High degree of polyclonality hinders somatic mutation calling in lung brush samples of COPD cases and controls.Scientific reports · 2019Article
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 3 institutions in 2 countries.
Funding
Abstract
Chronic obstructive pulmonary disease (COPD) patients are at increased risk of developing nonsmall cell lung carcinoma, irrespective of their smoking history. Although the mechanisms behind this observation are not clear, established drivers of carcinogenesis in COPD include oxidative stress and sustained chronic inflammation. Mitochondria are critical in these two processes and recent evidence links increased oxidative stress in COPD patients to mitochondrial damage. We therefore postulate that mitochondrial damage in COPD patients leads to increased oxidative stress and chronic inflammation, thereby increasing the risk of carcinogenesis.The functional state of the mitochondrion is dependent on the balance between its biogenesis and degradation (mitophagy). Dysfunctional mitochondria are a source of oxidative stress and inflammasome activation. In COPD, there is impaired translocation of the ubiquitin-related degradation molecule Parkin following activation of the Pink1 mitophagy pathway, resulting in excessive dysfunctional mitochondria. We hypothesise that deranged pathways in mitochondrial biogenesis and mitophagy in COPD can account for the increased risk in carcinogenesis. To test this hypothesis, animal models exposed to cigarette smoke and developing emphysema and lung cancer should be developed. In the future, the use of mitochondria-based antioxidants should be studied as an adjunct with the aim of reducing the risk of COPD-associated cancer.
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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.