Figure - PMC

Skip to main content

An official website of the United States government

Here's how you know

Here's how you know

Official websites use .gov
A .gov website belongs to an official government organization in the United States.

Secure .gov websites use HTTPS
A lock ( ) or https:// means you've safely connected to the .gov website. Share sensitive information only on official, secure websites.

View full-text article in PMC

. 2020 Oct 7;11:581300. doi: 10.3389/fimmu.2020.581300

Search in PMC
Search in PubMed
View in NLM Catalog
Add to search

Copyright © 2020 Wyczanska and Lange-Sperandio

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

PMC Copyright notice

Different outcomes of cell death and DAMP release due to urinary tract obstruction. Unilateral ureteral obstruction causes cell injury and necrosis, as well as the regulated forms necroptosis and pyroptosis. Due to cell stress and cell death DAMPs are released by injured endothelial (EC) and tubular epithelial (TEC) cells. These DAMPs activate PRRs such as TLRs on other cells. This can lead to further renal cell necrosis, with amplification of DAMPs. Fibroblasts and pericytes activated by DAMPs trigger fibrosis through proliferation, ECM secretion and myofibroblast transition. Activated dendritic cells (DC) and macrophages release cytokines and chemokines, which initiate an inflammatory response. IL-22 secreted by renal DCs, on the other hand, is able to activate the IL-22 receptor on TECs, which accelerates tubular re-epithelialization, thus promoting regeneration of TECs.