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 ANT1 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.
Dörner
Andrea
A
Charité-University Medicine, Campus Benjamin Franklin, Berlin, Germany. andrea.doerner@charite.de
Schultheiss
Heinz-Peter
HP
D000244:Adenosine Diphosphate; D000255:Adenosine Triphosphate; D017209:Apoptosis; D002318:Cardiovascular Diseases / Q000503:physiopathology*; D015870:Gene Expression; D006801:Humans; D000226:Mitochondrial ADP, ATP Translocases / Q000502:physiology*; D017202:Myocardial Ischemia / Q000503:physiopathology; D009206:Myocardium; D010085:Oxidative Phosphorylation
D000244:Adenosine Diphosphate; D000255:Adenosine Triphosphate; D000226:Mitochondrial ADP, ATP Translocases