ArticleBMC pulmonary medicine2016
Analysis of mitochondrial DNA alteration in new phenotype ACOS.
Article in BMC pulmonary medicine, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 34 citations in OpenAlex.
- Birch pollen allergen-induced dsDNA release activates cGAS-STING signaling and type 2 immune response in mice.iScience · 2025Article
- The Association Between Periodontal Inflamed Surface Area (PISA), Inflammatory Biomarkers, and Mitochondrial DNA Copy Number.Journal of clinical medicine · 2024Article
- Vitamin D ameliorates particulate matter induced mitochondrial damages and calcium dyshomeostasis in BEAS-2B human bronchial epithelial cells.Respiratory research · 2024Article
- The Asthma Risk Gene,Journal of respiratory biology and translational medicine · 2024Article
- Associations between mitochondrial biomarkers, urban residential exposures and childhood asthma outcomes over 6 months.Environmental research · 2023Article
- Sex-specific lung inflammation and mitochondrial damage in a model of electronic cigarette exposure in asthma.American journal of physiology. Lung cellular and molecular physiology · 2023Article
- Cytoplasmic DNAs: Sources, sensing, and roles in the development of lung inflammatory diseases and cancer.Frontiers in immunology · 2023Review
- Transcriptome analysis of sputum cells reveals two distinct molecular phenotypes of "asthma and chronic obstructive pulmonary disease overlap" in the elderly.European journal of medical research · 2022Article
- The Impact of Tobacco Cigarettes, Vaping Products and Tobacco Heating Products on Oxidative Stress.Antioxidants (Basel, Switzerland) · 2022Review
- Cellular Senescence in Aging Lungs and Diseases.Cells · 2022Review
- ACO (Asthma-COPD Overlap) Is Independent from COPD, a Case in Favor: A Systematic Review.Diagnostics (Basel, Switzerland) · 2021Review
- Dysregulated Cell Signaling in Pulmonary Emphysema.Frontiers in medicine · 2021Review
- Mitochondrial Dysfunction in Chronic Respiratory Diseases: Implications for the Pathogenesis and Potential Therapeutics.Oxidative medicine and cellular longevity · 2021Review
- Cellular stress responses and dysfunctional Mitochondrial-cellular senescence, and therapeutics in chronic respiratory diseases.Redox biology · 2020Review
- New Insights into the Implication of Mitochondrial Dysfunction in Tissue, Peripheral Blood Mononuclear Cells, and Platelets during Lung Diseases.Journal of clinical medicine · 2020Review
- Association of urine mitochondrial DNA with clinical measures of COPD in the SPIROMICS cohort.JCI insight · 2020Article
- Article
- Management of the Asthma-COPD Overlap Syndrome (ACOS): a Review of the Evidence.Current allergy and asthma reports · 2017Review
- Mitochondrial redox system, dynamics, and dysfunction in lung inflammaging and COPD.The international journal of biochemistry & cell biology · 2016Review
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundMitochondria contain their own DNA (MtDNA) that is very sensitive to oxidative stress and as a consequence could be damaged in quantity. Oxidative stress is largely recognized to play a key role in the pathogenesis of asthma and COPD and might have a role in the new intermediate phenotype ACOS (asthma-COPD overlap syndrome). The aim of this study was to investigate MtDNA alterations, as an expression of mitochondrial dysfunction, in ACOS and to verify whether they might help in the identification of this new phenotype and in its differentiation from asthma and COPD.
methodsTen (10) ACOS according to Spanish guidelines, 13 ACOS according to GINA guidelines, 13 COPD, 14 asthmatic patients and ten normal subjects were enrolled. They further underwent a blood, induced sputum and exhaled nitric oxide collection. Content of MtDNA and nuclear DNA (nDNA) were measured in the blood cells of patients by Real Time PCR.
resultsACOS patients showed an increase of MtDNA/nDNA ratio. Dividing ACOS according to guidelines, those from the Spanish showed a higher value of MtDNA/nDNA compared to those from GINA/GOLD (92.69 ± 7.31 vs 80.68 ± 4.16). Spanish ACOS presented MtDNA/nDNA ratio closer to COPD than asthma. MtDNA was higher in asthmatic, COPD, GINA and Spanish ACOS patients compared to healthy subjects (73.30 ± 4.47-137.0 ± 19.45-80.68 ± 4.16-92.69 ± 7.31 vs 65.97 ± 20.56).
conclusionWe found an increase of MtDNA/nDNA ratio in ACOS subjects that led us to conclude that there is presence of mitochondrial dysfunction in this disease, that makes it closer to COPD than to asthma. Although the MtDNA/nDNA ratio results are a useful marker for differential diagnosis from asthma, COPD and ACOS, further studies are needed to confirm the potentiality of MtDNA/nDNA ratio and to a better characterization of ACOS.
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