PI3K alpha is essential for the recovery from Cre/tamoxifen cardiotoxicity and in myocardial insulin signalling but is not required for normal myocardial contractility in the adult heart

摘要

Genetic mouse models have yielded conflicting conclusions about the role of PI3K alpha in heart physiology: specifically, the question of whether PI3K alpha has a direct role in regulating myocardial contractility. This has led to concerns that PI3K inhibitors currently in clinical trials for cancer may potentiate cardiotoxicity. Here we seek to clarify the role of PI3K alpha in normal heart physiology and investigate changes in related signalling pathways.