Deficiency of mindin reduces renal injury after ischemia reperfusion.

Tao BaiXiong WangCong QinKang YangZhiguo DuanZhixiu CaoJiaqian LiangLei WangJingdong YuanPengcheng Luo

Published in: Molecular medicine (Cambridge, Mass.) (2022)

These data demonstrate that mindin is a critical modulator of renal IR injury through regulating inflammatory responses. TLR4/JNK/NF-κB signaling most likely mediates the biological function of mindin in this model of renal ischemia.

Keyphrases

signaling pathway
toll like receptor
oxidative stress
cell death
nuclear factor
lps induced
induced apoptosis
pi k akt