TABLE 2.
Potential therapeutic targets/strategies in the pathogenesis of DN.
| Targets | Strategies | Mechanism of action | Effect on DN | References(s) |
|---|---|---|---|---|
| COX | COX-2 inhibition | Reduces glomerular hyperfiltration | Reduces glomerulosclerosis | Komers et al. (2001), Dey et al. (2004) |
| EP1 receptor inhibition | Inhibits transcriptional activation of TGF-β and fibronectin | Reduces mesangial expansion, improves kidney and glomerular hypertrophy | Makino et al. (2002) | |
| TX synthase inhibition | Decreases the production of plasminogen activator inhibitor-1 | Reduces the incidence of intraglomerular thrombi and glomerulosclerosis | Xu et al. (2006) | |
| TP receptor inhibition | Attenuates various markers of oxidative stress and inflammation | Improves histological changes | Xu et al. (2006) | |
| LOX | LOX inhibition | Reduces p38 MAPK protein and collagen a5(IV) mRNA in podocyte | Reduces ECM expansion, glomerular hypertrophy and albuminuria | Yuan et al. (2008) |
| CYP450 | CYP4A inhibition | Downregulates of Nox1 and Nox4 protein and mRNA expression and inhibits of NADPH oxidase activity | Attenuates albuminuria and reduces podocyte loss, apoptosis and foot process effacement | Williams et al. (2007) |