Enigmatic variations: The many facets of CFTR function in the heart

It has long been known that cardiac myocytes release ATP, and that the release of ATP is increased in response to hypoxia and ischaemia. The mechanisms underlying that release and its regulation, however, remain unclear. In this issue of Acta Physiologica, Wang and colleagues from the Ballard lab present intriguing new evidence of a role for the cystic fibrosis transmembrane conductance regulator (CFTR) in the release of ATP from cardiac myocytes in response to simulated ischaemia.