Center for Diabetes and Endocrine Research (CeDER)

Guillermo Vazquez, PhD.



Guillermo Vazquez, PhD. Assistant Professor in the Department of Physiology and Pharmacology.


Vazquez received his Ph.D. from the Universidad Nacional del Sur in Bahia Blanca, Argentina. Before he joined the University of Toledo College of Medicine in February 2007, he was a Research Fellow in the Calcium Regulation Group in the Laboratory of Signal Transduction at the National Institute of Environmental Health Sciences in North Carolina.

Dr. Vazquez focuses on the role of Ca2+-dependent signaling via Transient Receptor Potential Canonical (TRPC) channels in endothelial dysfunction/inflammation associated with atherosclerosis, a chronic inflammatory vascular disease that represents the leading cause of death in western societies and the main vascular complication of diabetes, metabolic syndrome and obesity. Mammalian TRPC proteins (TRPC1 through TRPC7) form channels typically activated downstream receptor-dependent stimulation of phosphoinositide-specific phospholipase C (PLC). They take part in the action of various PLC-coupled receptors for transmitters, peptides and growth factors that modulate diverse vascular functions, such as vascular tone and permeability, secretion, endothelial cell proliferation and apoptosis. Whereas the importance of the role of Ca2+ channels in endothelial cell physiology and pathophysiology has received increasing appreciation over the last decade, the current understanding of its role in the signaling pathways underlying inflammatory vascular disease is in its infancy. Dr. Vazquez’s group has recently pioneered the demonstration that endothelial TRPC3 is fundamental within the signaling underlying regulated expression of VCAM-1 and monocyte adhesion in response to pro-atherogenic factors, two critical events in early and advanced stages of atherosclerotic lesion development. These findings led to the generation of two novel mouse models of atherosclerosis with endothelial-specific gain- and loss-of-function for TRPC3. These new mouse models are essential in elucidating the impact of Ca2+ channel expression/function in the pathogenesis of atherosclerosis.

Dr. Vazquez has authored 56 peer-reviewed articles. His laboratory has been funded from grants from the American Heart Association and promises upcoming funding by the NIH.
Last Updated: 6/26/15