瞬时受体电位阳离子通道6与肾脏疾病关系的研究进展
[Research advances in the association between transient receptor potential cation channel 6 and kidney disease].
作者信息
Cao Shan, Liu Yun-Guang
机构信息
Graduate School of Youjiang University for Nationalities, Baise, Gangxi 533000, China.
出版信息
Zhongguo Dang Dai Er Ke Za Zhi. 2018 Jan;20(1):72-76. doi: 10.7499/j.issn.1008-8830.2018.01.015.
Abstract
Transient receptor potential cation channel 6 (TRPC6) is a member of the transient receptor superfamily encoded by the TRPC6 gene and is widely expressed in tissues and organs of the human body, especially in the glomerular podocytes. TRPC6 interacts with various slit diaphragm (SD) proteins including podocin, nephrin, ACTN4, and CD2AP to maintain the normal structure and function of glomerular podocytes. Foot process fusion caused by podocyte damage due to various factors is the most important morphological change in kidney disease. This article reviews the biological function of TRPC6 and its effect on kidney disease.
摘要
瞬时受体电位阳离子通道6（TRPC6）是由TRPC6基因编码的瞬时受体超家族成员，广泛表达于人体的组织和器官中，尤其是肾小球足细胞。TRPC6与多种裂孔隔膜（SD）蛋白相互作用，包括足突蛋白、nephrin、α-辅肌动蛋白4和CD2相关蛋白，以维持肾小球足细胞的正常结构和功能。由于各种因素导致足细胞损伤引起的足突融合是肾脏疾病中最重要的形态学变化。本文综述了TRPC6的生物学功能及其对肾脏疾病的影响。
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本文引用的文献
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Changes in podocyte TRPC channels evoked by plasma and sera from patients with recurrent FSGS and by putative glomerular permeability factors.由复发性 FSGS 患者的血浆和血清以及潜在的肾小球通透性因子引起的足细胞 TRPC 通道的变化。
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Inhibition of TRPC6 Signal Pathway Alleviates Podocyte Injury Induced by TGF-β1.抑制瞬时受体电位阳离子通道蛋白6信号通路可减轻转化生长因子-β1诱导的足细胞损伤。
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gene promoter polymorphisms in steroid resistant nephrotic syndrome children.激素抵抗型肾病综合征患儿的基因启动子多态性
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Inhibition of TRPC6 channels ameliorates renal fibrosis and contributes to renal protection by soluble klotho.抑制瞬时受体电位阳离子通道6（TRPC6）可改善肾纤维化，并有助于可溶性α-klotho发挥肾脏保护作用。
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