Deletion of lymphotoxin-β receptor (LTβR) protects against acute kidney injury by PPARα pathway.

ABSTRACT:

Background

Recent data has shown a considerable advancement in understanding the role of lymphotoxin-β receptor (LTβR) in inflammation. However, the functions and underlying mechanisms of LTβR in acute kidney injury (AKI) remain largely unknown.

Methods

AKI was induced in mice by renal ischemia-reperfusion (I/R). HK-2 cells and primary renal tubular epithelial cells (RTECs) were subjected to hypoxia/reoxygenation (H/R) injury. The effects of LTβR depletion were examined in mice, as well as primary RTECs. Bone marrow chimeric mice was generated to determine whether the involvement of LTβR expression by parenchymal cells or bone marrow derived cells contributes to renal injury during AKI. RNA sequencing techniques were employed to investigate the mechanism via which LTβR signa

SUBMITTER: Wang Z 

PROVIDER: S-EPMC11661049 | biostudies-literature | 2024 Dec

REPOSITORIES: biostudies-literature