Kathrin Banach, PhD

Banach’s research focuses on the cellular mechanism of atrial fibrillation (AF), the most common cardiac arrhythmia in clinical practice that can precipitate heart failure, stroke and even death. In an ongoing project, her team determined that the expression of the p21-activated kinase (Pak1) is decreased in the etiology of AF in patients and animal models of AF, and that attenuation of atrial Pak1 activity increases atrial arrhythmic activity. The current aims of her laboratory are to determine the molecular mechanisms involved in the following processes:

In a new collaborative project between basic researchers (Banach and Blatter) and clinical faculty (Feinstein and Okwuosa), an animal model is being developed to determine the molecular mechanism of chemotherapy-induced cardiotoxicity and to explore mechanisms of cardiac specific drug delivery for cardioprotection.