It is known that the reduced form of thioredoxins play a key role in the repair of oxidized proteins, and the fact that the AF + CE combination caused a shift of the mitochondrial Trx2 to oxidized form (Figure 5B) supports the hypothesis that AF + CE combination would lead to oxidative damage to mitochondrial redox-sensitive proteins and thus cause dysfunction of the mitochondrial respiratory chain. Here, TXN is linked to atrial fibrillation.