This project aims to evaluate cardioprotective mechanisms after AMI that are mediated by RKIP and its implications on β-adrenergic receptor (βAR) signaling. Mice with cardiomyocyte specific or ubiquitous overexpression of RKIP or RKIP knockout mice will be used. The phenotypic outcome in response to AMI will be characterized in dependency on the presence of β1- and β2AR and of a diabetic condition as an additional oxidative trigger and significant risk factor after AMI. Molecular analyses promise valuable insights in post-MI disease modulating processes that potentially involve βAR-mediated cardioprotection.
© HHU / Ivo Mayr
Tanitha Bettina Baumgarten