| Complication | Evidence | PMID |
| Nephropathy | 1. Losartan could suppress the expression of COX2 and TGF-beta1 in the kidney of DN rats and attenuate the renal lesions caused by DN. | 18812657 |
| Cardiovascular | 1. Specifically, SILD1) normalizes the frequency of circulating pro-inflammatory monocytes triggered by hyperglycemia (53.7 +- 7.9% of CD11b+Gr-1+ cells in STZ vs. 30.4 +- 8.3% in STZ+SILD and 27.1 +- 1.6% in CTRL, P<0.01); 2) prevents STZ-induced tissue inflammatory infiltration (4-fold increase in F4/80+ macrophages in diabetic vs. control mice) by increasing renal and heart anti-inflammatory TEMs (30.9 +- 3.6% in STZ+SILD vs. 6.9 +- 2.7% in STZ, P <0.01, and 11.6 +- 2.9% in CTRL mice); 3) reduces vascular inflammatory proteins (iNOS, COX2, VCAM-1) promoting tissue protection; 4) lowers monocyte adhesion to human endothelial cells in vitro through the TIE2 receptor. All these changes occurred independently from changes of glycemic status. | 25961566 |
| Retinopathy | 1. COX-2 contributes markedly to preretil neovascularization in ischemic retinopathies, and this effect seems to be Prostaglangin E2 (PGE2) mediated mostly via EP3receptors implicating a new interaction through TSP-1 and CD36 | 12821538 |
| Neuropathy | 1. These prelimiry data support the role of the activation of the COX-2 pathway in mediating sensory and motor nerve conduction velocity deficits in experimental diabetic neuropathy (EDN). These findings also suggest that the COX-2 pathway seems to be an important modulator of oxidative stress in EDN. | 16356116 |
