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The following is a summary of “Mitochondrial DNA copy number variation in asthma risk, severity, and exacerbations,” published in the April 2025 issue of Journal of Allergy and Clinical Immunology by Xu et al. 

Asthma involves mitochondrial dysfunction. A lower mitochondrial DNA copy number (mtDNA-CN) indicates impaired mitochondrial function. 

Researchers conducted a retrospective study to investigate the relationship between low mtDNA-CN and asthma diagnosis, severity, and exacerbations. 

They evaluated mtDNA-CN in blood samples from 2 cohorts: UK Biobank (UKB) (asthma, n = 39,147; no asthma, n = 302,302) and severe asthma research program (SARP) (asthma, n = 1,283; nonsevere asthma, n = 703) to assess its association with asthma status and severity. 

The results showed individuals with asthma had lower mtDNA-CN than those without asthma in UKB (β = −0.006 [95% CI, −0.008 to −0.003], P = 6.23 × 10⁻⁶). Lower mtDNA-CN was linked to asthma prevalence but not severity in UKB or SARP. mtDNA-CN declined with age but remained lower in asthma across all ages. In SARP, higher mtDNA-CN was linked to lower 1-year exacerbation risk (odds ratio (OR) = 0.333 [95% CI, 0.173 to 0.542], P = .001). Inflammation and oxidative stress markers were higher in asthma but did not explain lower mtDNA-CN. Mendelian randomization suggested a causal link between asthma-related genetic variants and mtDNA-CN. 

Investigators found mtDNA-CN was lower in asthma and associated with exacerbations. They also found this was not driven by inflammation but linked to genetic predisposition. 

Source: jacionline.org/article/S0091-6749(24)00906-0/abstract