Deficiency of C3a receptor attenuates the development of diabetic nephropathy.

ABSTRACT:

Objective

Diabetic nephropathy (DN) is the leading cause of chronic kidney disease and end-stage renal disease. Emerging evidence suggests that complement activation is involved in the pathogenesis of DN. The aim of this study was to investigate the pathogenic role of C3a and C3a receptor (C3aR) in DN.

Research design and methods

The expression of C3aR was examined in the renal specimen of patients with DN. Using a C3aR gene knockout mice (C3aR^-/-), we evaluated kidney injury in diabetic mice. The mouse gene expression microarray was performed to further explore the pathogenic role of C3aR. Then the underlying mechanism was investigated in vitro with macrophage treated with C3a.

Results

Compared with normal controls, the renal expression of C3aR was

SUBMITTER: Li XQ 

PROVIDER: S-EPMC6861086 | biostudies-literature | 2019

REPOSITORIES: biostudies-literature