ArticleThe Journal of allergy and clinical immunology2025
Mitochondrial DNA copy number variation in asthma risk, severity, and exacerbations.
Article in The Journal of allergy and clinical immunology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed.
- Histidine metabolic reprogramming drives oxidative stress induced mtDNA release to promote necroptosis and airway inflammation in severe asthma.Redox biology · 2026Article
- Fueling the fire: metabolic dysfunction and senescence as drivers of lung aging and disease.Physiological reviews · 2026Review
- Fueling asthma inflammation via bioenergetic metabolic reprogramming.Redox biology · 2026Article
- Targeted inhibition of ATP synthase subunit c by pp10-loaded inhalable albumin nanoparticles ameliorates airway inflammation in asthma.Journal of nanobiotechnology · 2026Article
- Regulation of mitochondrial function during spermatogenesis and sperm maturation.Cellular & molecular biology letters · 2026Review
- Unraveling the telomere-mitochondrial axis in colorectal cancer: Results from a prospectively followed cohort.Molecular medicine (Cambridge, Mass.) · 2026Article
- Mitochondrial haplogroup M contributes to asthma risk in the Kuwaiti population.Frontiers in allergy · 2025Article
- Role of Paraoxonase 2 in Airway Epithelial Response to Oxidant Stress.Antioxidants (Basel, Switzerland) · 2024Article
- White Matter Imaging Phenotypes Mediate the Negative Causality of Mitochondrial DNA Copy Number on Sleep Apnea: A Bidirectional Mendelian Randomization Study and Mediation Analysis.Nature and science of sleep · 2024Article
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24 authors.
Funding
Abstract
backgroundAsthma pathophysiology is associated with mitochondrial dysfunction. Mitochondrial DNA copy number (mtDNA-CN) has been used as a proxy of mitochondrial function, with lower levels indicating mitochondrial dysfunction in population studies of cardiovascular diseases and cancers.
objectivesWe investigated whether lower levels of mtDNA-CN are associated with asthma diagnosis, severity, and exacerbations.
methodsmtDNA-CN is evaluated in blood from 2 cohorts: UK Biobank (UKB) (asthma, n = 39,147; no asthma, n = 302,302) and Severe Asthma Research Program (SARP) (asthma, n = 1283; nonsevere asthma, n = 703).
resultsIndividuals with asthma have lower mtDNA-CN compared to individuals without asthma in UKB (beta, -0.006 [95% confidence interval, -0.008 to -0.003], P = 6.23 × 10
conclusionmtDNA-CN is lower in asthma than in no asthma and is associated with exacerbations. Low mtDNA-CN in asthma is not mediated through inflammation but is associated with a genetic predisposition to asthma.
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