C3 glomerulopathy (C3G)

Panel A Study design for evaluating the efficacy of anti-hC3 siRNA in the B6‑hC3/mC3‑KO spontaneous C3G model.

Panel B Serum levels of human C3, C3a, and Ba/CFB were elevated in the model group, and this upregulation was reversed upon anti‑hC3 siRNA treatment.

Panel C-E The UACR, kidney-to-body weight ratio, and renal hC3-positive staining were markedly increased in the model group, and anti‑hC3 siRNA treatment alleviated these pathological phenotypes.

Statistical analysis was performed using one‑way ANOVA, and all data presented as mean ± SEM. *p<0.05, **p<0.01, ***p<0.001,****p<0.0001. This study was collaborated with third party. 

Panel A B6 and B6-CFH KO mice were induced with anti-GBM to establish C3G disease model.

Panel B Compared with B6 mice, B6-CFH KO mice exhibited lower mouse C3 levels in both males and females.

Panel C-D In both sexes, urine protein indices (UACR and UPCR), as well as serum BUN and CREA, increased gradually over time after anti-GBM treatment in B6-CFH KO mice, but not in B6 mice.

Panel E Pathological examination revealed aggravated renal pathological lesions in B6-CFH KO mice following anti-GBM treatment, indicating the development of glomerulonephritis in these mice.

Statistical analysis was performed using one‑way ANOVA, and all data presented as mean ± SEM. *p<0.05, **p<0.01, ***p<0.001,****p<0.0001.