Identifies a mechanistic link between oxidative stress, mitochondrial dysfunction, and AF susceptibility in Pitx2-deficient mice, highlighting potential genotype-specific therapeutic targets.
These results demonstrate a critical role for lipid dicarbonyl mediators of oxidative stress in the proarrhythmic remodeling and AF susceptibility that occurs with Pitx2 deficiency, implying the possibility of genotype-specific therapy to prevent AF.
Subati et al. (Mon,) studied this question.