Activated WNK3 induced by intracerebral hemorrhage deteriorates brain injury maybe via WNK3/SPAK/NKCC1 pathway.

CONCLUSIONS: In conclusion, our findings showed that WNK3 and WNK3/SPAK/NKCC1 signaling pathway play a vital biological function in ICH-induced SBI. Depletion of WNK3 attenuated brain injury after ICH both in vivo and in vitro. Thus, WNK3 and WNK3/SPAK/NKCC1 signaling pathway are potential targets for treating SBI after ICH.
PMID: 32589890 [PubMed - as supplied by publisher]

Source: Experimental Neurology - June 22, 2020 Category: Neurology Authors: Wu D, Lai N, Deng R, Liang T, Pan P, Yuan G, Li X, Li H, Shen H, Wang Z, Chen G Tags: Exp Neurol Source Type: research