Transgenic catalase mice |
Reduced albuminuria, glomerulosclerosis, interstitial fibrosis and tubular apoptosis [59, 60] |
Catalase-deficient mice |
Kidneys are more prone to oxidative stress [61] |
HO-1 gene transfer in mice or rats |
Reduced apoptosis and kidney injury [63] |
HO-2-deficient mice |
Enhanced STZ-induced diabetic nephropathy, which could be restored by HO-1 gene transfer [64] |
SOD transgenic mice |
Protection against diabetic nephropathy [68] |
Thioredoxin-1 transgenic mice |
Diminished albuminuria and tubular apoptosis [67] |
Peroxiredoxin-3 transgenic mice |
Protection against hyperglycemia and glucose intolerance and reduced fibroblast apoptosis by reducing mitochondrial H2O2 production [69] |
Glutathione peroxidase-1-deficient mice |
No effects on T1DM-induced kidney injury [70] |
Mice with a reduction of thrombo-modulin-dependent protein C activation |
Aggravated glomerular apoptosis and diabetic nephropathy [19, 56] |
Mice expressing a hyper-activatable protein C mutation |
Protein C activation prevents glomerular apoptosis and diabetic nephropathy [19, 56] |