LINC00355 mediates CTNNBIP1 promoter methylation and promotes ER stress-induced podocyte injury in diabetic nephropathy.
LINC00355 mediates CTNNBIP1 promoter methylation and promotes ER stress-induced podocyte injury in diabetic nephropathy.
复制标题
LINC00355 介导 CTNNBIP1 启动子甲基化并促进糖尿病肾病中 ER 应激诱导的足细胞损伤。
DOI：
10.1089/ars.2021.0227
复制
发表时间：
2023
影响因子：
6.6
通讯作者：
Xiao
中科院分区：
文献类型：
--
作者：
Tingting Zhang;Yan Zhang;Haosen Xu;Jin;Zhonglin Feng;Renwei Huang;Jian Geng;H. Chi;Xiao
目标
AIMS
Endoplasmic reticulum stress (ER stress) plays an important role in podocyte injury in diabetic nephropathy. Wnt/β-catenin signaling modulates ER stress, yet the epigenetic regulation of β-catenin in ER stress and podocyte injury remains largely unknown. Herein, we tested the hypothesis that LINC00355 recruits EZH1 to the promoter region of CTNNBIP1 and trimethylates H3K4 to regulate ER-stress induced podocyte injury in DN.
RESULTS
LINC00355 is upregulated in podocytes and correlates with renal function decline in DN patients. LINC00355 localizes in the nucleus and exerts biological functions by directly binding EZH1, which epigenetically targets CTNNBIP1 through repressive trimethylation of H3K4 and activates Wnt/β-catenin signaling and ER stress. Further, we provide mechanistic evidences that LINC00355 recruits EZH1 to the promoter region of CTNNBIP1 and regulates ER-stress induced podocyte injury in DN.
INNOVATION AND CONCLUSION
Our data reveal a major role of LINC00355/EZH1/CTNNBIP1 network in triggering podocyte injury, providing new evidences for understanding the role of ER stress in DN.
DOI：
10.1038/s41572-020-0196-7
发表时间：
2020-08-13
期刊：
Nature reviews. Disease primers
影响因子：
--
作者：
Kopp JB;Anders HJ;Susztak K;Podestà MA;Remuzzi G;Hildebrandt F;Romagnani P
通讯作者：
Romagnani P