N-type Calcium Channel and Renal Injury

Overview

Journal Int Urol Nephrol

Publisher Springer

Specialty Nephrology

Date 2022 Apr 13

PMID 35416563

Authors

Lei Bai

Shichao Sun

Yao Sun

Fujun Wang

Akira Nishiyama

Affiliations

Soon will be listed here.

Abstract

Accumulating evidences indicated that voltage-gated calcium channels (VDCC), including L-, T-, N-, and P/Q-type, are present in kidney and contribute to renal injury during various chronic diseases trough different mechanisms. As a voltage-gated calcium channel, N-type calcium channel was firstly been founded predominately distributed on nerve endings which control neurotransmitter releases. Since sympathetic nerve is distributed along renal afferent and efferent arterioles, N-type calcium channel blockade on sympathetic nerve terminals would bring renal dynamic improvement by dilating both arterioles and reducing glomerular pressure. In addition, large body of scientific research indicated that neurotransmitters, such as norepinephrine, releases by activating N-type calcium channel can trigger inflammatory and fibrotic signaling pathways in kidney. Interestingly, we recently demonstrated that N-type calcium channel is also expressed on podocytes and may directly contribute to podocyte injury in denervated animal models. In this paper, we will summarize our current knowledge regarding renal N-type calcium channels, and discuss how they might contribute to the river that terminates in renal injury.

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