Endothelial TRPC3/6/7 proteins at the edge of cardiovascular disease.
An impressive amount of experimental evidence accumulated over the last two decades has clearly demonstrated that Ca(2+) influx through plasma membrane Ca(2+)-permeable channels plays a critical role in endothelial cell physiology and pathophysiology. Research efforts aimed at understanding the role of Ca(2+) influx within the signaling events underlying endothelial dysfunction have grown at a fast pace over more recent years. Transient Receptor Potential Canonical (TRPC) proteins, which belong to the larger TRP superfamily of channel forming proteins, form Ca(2+)-permeable cation channels in vascular endothelium and there is currently no question about their involvement in Ca(2+) influx associated with endothelial cell's physiology. It is also becoming evident that TRPCs are important players in the pathogenesis of cardiovascular disease. Therefore, it is imperative to elucidate the mechanism/s underlying regulation of endothelial TRPC channels as well as to identify signaling events downstream TRPC activation in order to better comprehend their role in cardiovascular physiology and disease. This review focuses on members of the TRPC3/6/7 group of TRPC proteins, revises current knowledge on their expression and regulation in endothelium, and discusses their role in cardiovascular disease as it relates to endothelial dysfunction.
Tano
J Y
JY
Department of Physiology and Pharmacology, Center for Diabetes and Endocrine Research, College of Medicine, University of Toledo Health Science Campus, 3000 Arlington Ave., Toledo, OH 43614-5804, USA.
Smedlund
K
K
Vazquez
G
G
D000818:Animals; D002318:Cardiovascular Diseases / Q000235:genetics / Q000378:metabolism*; D004727:Endothelium / Q000378:metabolism*; D006801:Humans; D050051:Transient Receptor Potential Channels / Q000235:genetics / Q000378:metabolism*
D050051:Transient Receptor Potential Channels