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Heart disease is commonly associated with altered mitochondrial function and signs of oxidative stress. This study elucidates whether primary cardiac mitochondrial dysfunction causes changes in cardiomyocyte handling of reactive oxygen species (ROS) and Ca(2+). We used a mouse model with a tissue-specific ablation of the recently discovered mtDNA transcription regulator Mterf3 (Mterf3 KO). These mice display a cardiomyopathy with severe respiratory chain dysfunction, cardiac hypertrophy, and shortened lifespan. ROS and Ca(2+) handling were measured using fluorescent indicators and confocal microscopy.

Enhanced Cardiomyocyte Ca2+ Cycling Precedes Terminal AV-Block in Mitochondrial Cardiomyopathy Mterf3 KO Mice

Enhanced Cardiomyocyte Ca²⁺ Cycling Precedes Terminal AV-Block in Mitochondrial Cardiomyopathy Mterf3 KO Mice