Khayyat Naghmeh Hassanzadeh, Tomilin Viktor N, Zaika Oleg, Pochynyuk Oleh
Department of Integrative Biology and Pharmacology, The University of Texas Health Science Center at Houston , Houston, TX, USA.
Channels (Austin). 2020 Dec;14(1):257-267. doi: 10.1080/19336950.2020.1804153.
TRPC3 is a Ca-permeable cation channel commonly activated by the G-protein coupled receptors (GPCR) and mechanical distortion of the plasma membrane. TRPC3-mediated Ca 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.
瞬时受体电位通道3（TRPC3）是一种钙离子通透的阳离子通道，通常由G蛋白偶联受体（GPCR）和质膜的机械变形激活。TRPC3介导的钙离子内流参与了可兴奋细胞和非可兴奋细胞中的多种信号转导过程。肾脏在维持全身稳态和调节血压方面起着主导作用。TRPC3在肾血管系统和上皮细胞中大量表达，在这些部位它能够很好地介导信号转导并响应GPCR依赖的内分泌刺激发挥转运功能。此外，肾小管液流和渗透压的动态变化所产生的机械力可激活TRPC3。本文综述批判性地分析了已发表的关于TRPC3在肾脏不同部位生理作用的现有证据，并描述了TRPC3缺失的病理生理后果。我们还推测了如何将这些证据进一步转化应用于临床。
