Bone Marrow-Derived RIPK3 Mediates Kidney Inflammation in Acute Kidney Injury.

ABSTRACT:

Background

Receptor-interacting protein kinase 3 (RIPK3), a component of necroptosis pathways, may have an independent role in inflammation. It has been unclear which RIPK3-expressing cells are responsible for the anti-inflammatory effect of overall Ripk3 deficiency and whether Ripk3 deficiency protects against kidney inflammation occurring in the absence of tubular cell death.

Methods

We used chimeric mice with bone marrow from wild-type and Ripk3-knockout mice to explore RIPK3's contribution to kidney inflammation in the presence of folic acid-induced acute kidney injury AKI (FA-AKI) or absence of AKI and kidney cell death (as seen in systemic administration of the cytokine TNF-like weak inducer of apoptosis [TWEAK]).

Results

Tubular and interst

SUBMITTER: Martin-Sanchez D 

PROVIDER: S-EPMC8819996 | biostudies-literature | 2022 Feb

REPOSITORIES: biostudies-literature