Bs-526-04 impaired redox response to increased workload in atrial mitochondria from patients with atrial fibrillation

Calcium handling abnormalities contribute to the pathophysiology of atrial fibrillation (AF). In ventricular myocytes, Ca2+ has been shown to play an important role in mitochondrial response to increased workload by activating key dehydrogenases in the Krebs cycle, necessary for NAD(P)H regeneration and, ultimately, neutralisation.