Åsa B. Gustafsson

TL;DR: The data suggest that anthracycline treatment impairs vascular development as well as progenitor cell function in the young heart, resulting in an adult heart that is more susceptible to stress.

TL;DR: It is suggested that Bnip3 mediates mitochondrial dysfunction through activation of Bax or Bak which is independent of mPTP opening.

TL;DR: The results support a model where Bnip3 induces selective removal of the mitochondria in cardiac myocytes, and that BnIP3 triggers induction of autophagy independent of Ca2+, ROS generation, and mPTP opening.

TL;DR: The literature is reviewed and the evidence that autophagy can have both beneficial and detrimental roles in the myocardium depending on the level of Autophagy is discussed, and potential mechanisms by which autophagic provides protection in cells are discussed.

TL;DR: It is shown that transduction of TAT-ARCL31F, a mutant of ARC in the caspase recruitment domain, did not reduce creatine kinase release and infarct size after I/R, and ARC can protect against cell death by interfering with activation of the mitochondrial death pathway through the interaction with Bax, preventing mitochondrial dysfunction and release of pro-apoptotic factors.