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Education and Training
I received my MD from the Technical University in Aachen in Germany and went on to train in Internal Medicine and Cardiology at the University of Aachen Medical School. I received my PhD in cardiovascular physiology from Maastricht University in the Netherlands. I then moved to the University of Maryland to train with Dr. Lederer, where I was appointed Research Associate in 2014.
Dr. Greiser's work centers on investigating cardiac calcium signaling and cellular electrophysiology with a focus on the atria in health and disease. Past and present work has addressed changes specific to Atrial Fibrillation, the most common arrhythmia in men. Dr. Greiser has discovered the concept of “Calcium signaling silencing” in atrial mycocytes as a response to rapid atrial activation. This novel concept is an important adaptive mechanisms after the initiation of atrial fibrillation which protects the atrial myocytes from intracellular calcium overload.
Dr. Greiser has developed and implemented novel imaging techniques, most of which are designed for investigating calcium signals at high temporal and spatial resolution in isolated atrial myocytes. In addition to the effort to develop new tools he has extensively collaborated with many other investigators to implement these new tools in their ongoing investigations.
Atrial Fibrillation: Calcium Imaging
1. Calcium Signaling Silencing in Atrial Fibrillation
Greiser M. J Physiology. 2017, doi: 10.1113/JP273045. [Epub ahead of print]
2. Tachycardia-induced Silencing of Subcellular Ca2+ Signaling in Atrial Myocytes.
Greiser M, Kerfant BG, Williams GS, Voigt N, Harks E, Dibb KM, Giese A, Meszaros J, Verheule S, Ravens U, Allessie MA, Gammie JS, van der Velden J, Lederer WJ, Dobrev D, Schotten U. J Clin Investigation. 2014;124(11):4759-72.
3. Dynamic Remodeling of Intracellular Ca2+ Signaling during Atrial Fibrillation.
Greiser M, Schotten. J Mol Cell Cardiol, 2013;58: 134-42.
My research focuses on the molecular and cellular mechanisms underlying Atrial Fibrillation. Specifically, I am interested in changes in the intracellular [Ca2+] and [Na+] homeostasis that underlie arrhythmogenic mechanisms in Atrial Fibrillation. I am using state of the art confocal laser scanning microscopy to image intracellular Ca2+ microdomains in viable atrial myocytes. To address different arrhythmia mechanisms we work with various types of atrial fibrillation animal models. We were the first to characterize significant changes in the intracellular [Na+] homeostasis as a response to rapid atrial activation and current research focusses on the regulatory changes in atrial [Na+] homeostasis during atrial fibrillation.