Adenine nucleotide translocase in the focus of cardiovascular diseases

Adenine nucleotide translocase (ANT) facilitates the exchange of extramitochondrial adenosine diphosphate and intramitochondrial adenosine triphosphate across the inner mitochondrial membrane and appears to be a member of the mitochondrial permeability transition pore whose opening induces apoptosis. Genetically or physiologically restricted ANT function associated with insufficient energy supply and induced apoptosis leads to severe cardiac disturbance. In contrast, to counter myocardial stress, heart tissue developed cell protecting gene programs including ANTI up-regulation to stabilize energy supply and concurrently suppress apoptotic processes. This review describes characteristics of ANT function and expression in cardiovascular diseases and ANT's role in cardioprotection.