showed that the upregulation of C3a/C3aR and C5a/C5aR was associated with endothelial–myofibroblast transition (EndMT) and fibrosis in glomerular endothelial cells of DKD patients and diabetic rats, and the specific receptor antagonists C3aRA/C5aRA could ameliorate EndMT and renal fibrosis via the inhibition of the Wnt/β-catenin pathway both in vitro and in vivo (50). Here, C3 is linked to diabetic kidney disease.