Our lab studies cellular signaling pathways that affect vascular wall physiology and disease. In particular, we are interested in signaling regulators that integrate increased Calcium- signaling and reactive oxygen species-dependent signaling. Currently, we focus on the role of the multifunctional Ca2+/calmodulin dependent protein kinase II (CaMKII). Our lab established that CaMKII in mitochondria of smooth muscle ad endothelial cells controls Ca2+ uptake into mitochondria via the mitochondrial Ca2+ uniporter.

Work from the Grumbach laboratory led to current concepts on the role of the multifunctional Ca2+/calmodulin dependent protein kinase II (CaMKII) about as a signal contributing to clinically relevant vascular disease. The laboratory work ranges from elucidating signaling pathways controlled by CaMKII to systems physiology using genetically modified mice. The main research themes pursued by the Grumbach laboratory are:

1. Impact of mitochondria in smooth muscle cells on vascular wall remodeling after injury

2. Mitochondrial smooth muscle cell biology in type 2 diabetes

3. Mitochondrial Ca2+ handling in hypertension

4. Mechanisms of endothelial damage by chemo- and radiation therapy