Abstract
Transient receptor potentials (TRPs) are non-selective cation channels that are widely expressed in vascular beds. They contribute to the Ca2+ influx evoked by a wide spectrum of chemical and physical stimuli, both in endothelial and vascular smooth muscle cells. Within the superfamily of TRP channels, different isoforms of TRPC (canonical) and TRPV (vanilloid) have emerged as important regulators of vascular tone and blood flow pressure. Additionally, several lines of evidence derived from animal models, and even from human subjects, highlighted the role of TRPC and TRPV in vascular remodeling and disease. Dysregulation in the function and/or expression of TRPC and TRPV isoforms likely regulates vascular smooth muscle cells switching from a contractile to a synthetic phenotype. This process contributes to the development and progression of vascular disorders, such as systemic and pulmonary arterial hypertension, atherosclerosis and restenosis. In this review, we provide an overview of the current knowledge on the implication of TRPC and TRPV in the physiological and pathological processes of some frequent vascular diseases.
Highlights
Blood vessels are composed essentially of two interacting cell types: endothelial cells (ECs) from the tunica intima lining of the vessel wall and vascular smooth muscle cells (VSMCs) from tunica media of the vascular tube
This finding was supported by Schnitzler et al [35], who proposed that TRPC6 is important to the myogenic response, not as a mechanosensitive channel but as a channel activated by G-protein coupled receptors [35]
Vascular injury is characterized by an endothelial denudation that leads an inflammatory response; this results in the onset of several proliferative processes, including VMSCs switching from contractile to synthetic phenotypes, which contributes to the development and progression of restenosis [128,129]
Summary
Blood vessels are composed essentially of two interacting cell types: endothelial cells (ECs) from the tunica intima lining of the vessel wall and vascular smooth muscle cells (VSMCs) from tunica media of the vascular tube. The endothelium is the primary tissue responsible for the regulation of VSMCs’ contractility, vascular wall permeability, angiogenesis, triggering coagulation and fibrinolysis and the regulation of the vascular tone and vessels diameter, as reviewed in [13,14]. In all these mechanism, endothelium production of nitric oxide (NO), prostaglandin and the secretion of vasoactive agonists play a critical role [15]. We will focus in particular on the roles of TRPC and TRPV, which are among the most important TRPs in vascular beds
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