ABSTRACT

TRPC3 is a Ca²⁺-permeable cation channel commonly activated by the G-protein coupled receptors (GPCR) and mechanical distortion of the plasma membrane. TRPC3-mediated Ca²⁺ influx has been implicated in a variety of signaling processes in both excitable and non-excitable cells. Kidneys play a commanding role in maintaining whole-body homeostasis and setting blood pressure. TRPC3 is expressed abundantly in the renal vasculature and in epithelial cells, where it is well positioned to mediate signaling and transport functions in response to GPCR-dependent endocrine stimuli. In addition, TRPC3 could be activated by mechanical forces resulting from dynamic changes in the renal tubule fluid flow and osmolarity. This review critically analyzes the available published evidence of the physiological roles of TRPC3 in different parts of the kidney and describes the pathophysiological ramifications of TRPC3 ablation. We also speculate how this evidence could be further translated into the clinic.

摘要

TRPC3是一个Ca ²⁺渗透性阳离子通道，通常由G蛋白偶联受体（GPCR）和质膜的机械变形激活。TRPC3介导的Ca ²⁺在可兴奋和不可兴奋的细胞中，潮气都与多种信号传导过程有关。肾脏在维持全身稳态和调节血压中起着重要作用。TRPC3在肾血管和上皮细胞中大量表达，在此位置上它可以很好地介导响应GPCR依赖的内分泌刺激的信号传导和转运功能。此外，TRPC3可以由肾小管液流和渗透压的动态变化产生的机械力激活。这篇评论严格分析了TRPC3在肾脏不同部位的生理作用的可用公开证据，并描述了TRPC3消融的病理生理后果。我们还推测如何将这些证据进一步转化为临床。