title: Role of TRP channels in the cardiovascular system.
abstract: The transient receptor potential (TRP) superfamily consists of a large number of nonselective cation channels with variable degree of Ca(2+)-permeability. The 28 mammalian TRP channel proteins can be grouped into six subfamilies: canonical, vanilloid, melastatin, ankyrin, polycystic, and mucolipin TRPs. The majority of these TRP channels are expressed in different cell types including both excitable and nonexcitable cells of the cardiovascular system. Unlike voltage-gated ion channels, TRP channels do not have a typical voltage sensor, but instead can sense a variety of other stimuli including pressure, shear stress, mechanical stretch, oxidative stress, lipid environment alterations, hypertrophic signals, and inflammation products. By integrating multiple stimuli and transducing their activity to downstream cellular signal pathways via Ca(2+) entry and/or membrane depolarization, TRP channels play an essential role in regulating fundamental cell functions such as contraction, relaxation, proliferation, differentiation, and cell death. With the use of targeted deletion and transgenic mouse models, recent studies have revealed that TRP channels are involved in numerous cellular functions and play an important role in the pathophysiology of many diseases in the cardiovascular system. Moreover, several TRP channels are involved in inherited diseases of the cardiovascular system. This review presents an overview of current knowledge concerning the physiological functions of TRP channels in the cardiovascular system and their contributions to cardiovascular diseases. Ultimately, TRP channels may become potential therapeutic targets for cardiovascular diseases.
authors.affiliation: Calhoun Cardiology Center, Department of Cell Biology, University of Connecticut Health Center, Farmington, Connecticut.
authors.forename: Zhichao
authors.initials: Z
authors.lastname: Yue
authors.affiliation: Calhoun Cardiology Center, Department of Cell Biology, University of Connecticut Health Center, Farmington, Connecticut.
authors.forename: Jia
authors.initials: J
authors.lastname: Xie
authors.affiliation: Calhoun Cardiology Center, Department of Cell Biology, University of Connecticut Health Center, Farmington, Connecticut.
authors.forename: Albert S
authors.initials: AS
authors.lastname: Yu
authors.affiliation: Calhoun Cardiology Center, Department of Cell Biology, University of Connecticut Health Center, Farmington, Connecticut.
authors.forename: Jonathan
authors.initials: J
authors.lastname: Stock
authors.affiliation: Calhoun Cardiology Center, Department of Cell Biology, University of Connecticut Health Center, Farmington, Connecticut.
authors.forename: Jianyang
authors.initials: J
authors.lastname: Du
authors.affiliation: Calhoun Cardiology Center, Department of Cell Biology, University of Connecticut Health Center, Farmington, Connecticut lyue@uchc.edu.
authors.forename: Lixia
authors.initials: L
authors.lastname: Yue
mesh_terms: D000818:Animals; D002319:Cardiovascular System / Q000254:growth & development / Q000378:metabolism*; D006331:Heart Diseases / Q000235:genetics / Q000378:metabolism*; D006801:Humans; D015398:Signal Transduction; D050051:Transient Receptor Potential Channels / Q000737:chemistry / Q000235:genetics / Q000378:metabolism*
chemical_list: D050051:Transient Receptor Potential Channels
keywords: Ca2+ signaling; TRP channels; heart diseases; pathogenesis; vascular disorders