Ion channels as a therapeutic target for renal fibrosis.
Ion channels as a therapeutic target for renal fibrosis.
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离子通道作为肾纤维化的治疗靶点
DOI：
10.3389/fphys.2022.1019028
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发表时间：
2022
影响因子：
4
通讯作者：
中科院分区：
文献类型：
--
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肾脏离子通道转运和电解质紊乱在肾脏功能损害和纤维化过程中起重要作用。众所周知，用于治疗肾纤维化的有效药物有限，并且由于大量离子通道参与肾纤维化过程，因此理解离子通道转运机制以及它们之间的信号级联的复杂网络对于确定减缓肾纤维化的潜在治疗方法至关重要。本文就离子通道在肾纤维化中的作用作一综述。我们密切关注囊性纤维化跨膜传导调节因子（CFTR）、跨膜成员16 A（TMEM 16 A）和其他Cl−通道介导的信号通路和离子浓度对纤维化的影响，以及Ca 2+处理通道（包括Ca 2+释放激活的Ca 2+通道（CRAC）、嘌呤能受体和瞬时受体电位（TRP）通道）作用的各种复杂机制。此外，我们还重点研究了上皮钠通道（ENaC）、Na+，K+-ATP酶、Na+-H+交换器等Na+转运系统以及钙激活的K+通道、电压依赖性K+通道、ATP敏感性K+通道等K+通道在肾纤维化中的作用。通过进一步剖析这些机制提出的潜在治疗方法可能会提供新的治疗机会，以减少慢性肾脏疾病的负担。
Renal ion channel transport and electrolyte disturbances play an important role in the process of functional impairment and fibrosis in the kidney. It is well known that there are limited effective drugs for the treatment of renal fibrosis, and since a large number of ion channels are involved in the renal fibrosis process, understanding the mechanisms of ion channel transport and the complex network of signaling cascades between them is essential to identify potential therapeutic approaches to slow down renal fibrosis. This review summarizes the current work of ion channels in renal fibrosis. We pay close attention to the effect of cystic fibrosis transmembrane conductance regulator (CFTR), transmembrane Member 16A (TMEM16A) and other Cl− channel mediated signaling pathways and ion concentrations on fibrosis, as well as the various complex mechanisms for the action of Ca2+ handling channels including Ca2+-release-activated Ca2+ channel (CRAC), purinergic receptor, and transient receptor potential (TRP) channels. Furthermore, we also focus on the contribution of Na+ transport such as epithelial sodium channel (ENaC), Na+, K+-ATPase, Na+-H+ exchangers, and K+ channels like Ca2+-activated K+ channels, voltage-dependent K+ channel, ATP-sensitive K+ channels on renal fibrosis. Proposed potential therapeutic approaches through further dissection of these mechanisms may provide new therapeutic opportunities to reduce the burden of chronic kidney disease.
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影响因子：
5
作者：
Adapala RK;Thoppil RJ;Luther DJ;Paruchuri S;Meszaros JG;Chilian WM;Thodeti CK
通讯作者：
Thodeti CK
TRPV1 通道在缺血/再灌注引起的急性肾损伤中的作用。
影响因子：
3.7
作者：
Chen L;Markó L;Kaßmann M;Zhu Y;Wu K;Gollasch M
通讯作者：
Gollasch M
影响因子：
5.6
作者：
Catacuzzeno, Luigi;Aiello, Francesco;Franciolini, Fabio
通讯作者：
Franciolini, Fabio
影响因子：
29.4
作者：
Benedetti, A;Di Sario, A;Svegliati-Baroni, G
通讯作者：
Svegliati-Baroni, G
影响因子：
10
作者：
Cruse, G.;Duffy, S. M.;Bradding, P.
通讯作者：
Bradding, P.