Farnesoid X receptor promotes renal ischaemia‐reperfusion injury by inducing tubular epithelial cell apoptosis

• DOI: 10.1111/cpr.13005
• Publication Date: 2021-02-20T07:14:10Z
• Authors: Yao Xu; Dawei Li; Jiajin Wu; Minfang Zhang; Xinghua Shao; Longmei Xu; Lumin Tang; Minyan Zhu; Zhaohui Ni; Ming Zhang; Shan Mou
• Keywords: Farnesoid X receptor

Abstract Purpose We investigated the role of farnesoid X receptor (FXR), a ligand‐dependent transcription factor, in renal ischaemia‐reperfusion (I/R) injury. Materials and Methods performed unilateral I/R model FXR knockout ( Fxr −/− ) wild‐type (WT) mice vivo hypoxia‐reoxygenation (H/R) vitro. The pathways by which induces apoptosis were detected using proteome profiler array. effects on evaluated immunoblotting, TUNEL assays flow cytometry. Results Compared with WT mice, showed improved function reduced tubular injury scores apoptosis. Consistent results, silencing decreased number apoptotic HK‐2 cells after H/R, while overexpression aggravated Notably, bone marrow transplantation (BMT) immunohistochemistry experiments revealed involvement epithelium rather than inflammatory cells. Furthermore, vitro studies demonstrated that deficiency increased phosphorylated Bcl‐2 agonist cell death (p‐Bad) expression levels ratio Bcl‐2/Bcl‐xL to Bax kidney. Treatment wortmannin, p‐Bad expression, inhibited eliminated tolerance mouse kidneys Conclusions These results established pivotal importance inactivation epithelial may promote inhibiting PI3k/Akt‐mediated Bad phosphorylation cause damage.