| First Author | Lenoir O | Year | 2017 |
| Journal | J Diabetes Res | Volume | 2017 |
| Pages | 9603924 | PubMed ID | 29359167 |
| Mgi Jnum | J:273569 | Mgi Id | MGI:6282759 |
| Doi | 10.1155/2017/9603924 | Citation | Lenoir O, et al. (2017) Hmox1 Deficiency Sensitizes Mice to Peroxynitrite Formation and Diabetic Glomerular Microvascular Injuries. J Diabetes Res 2017:9603924 |
| abstractText | Objective: Indirect evidence suggests a role for heme oxygenase-1 (HO-1) in limiting diabetic vasculopathy. The goal of this study was to assess the role of HO-1 in the development of microvascular lesions within glomeruli during diabetes mellitus using a mouse model with specific alteration of the Hmox1 gene. Approach and Results: The effects of Hmox1 haploinsufficiency were studied as a means of assessing the intrinsic contribution of HO-1 in the development of renal microvascular lesions during diabetes. Renal function and histology were analyzed 10 weeks after diabetes induction with streptozotocin. Diabetic Hmox1(+/-) mice showed higher levels of albuminuria and blood urea compared to their wild-type diabetic littermates. More severe glomerular microvascular lesions were also observed in the diabetic Hmox1(+/-) mice. This was associated with a renal increase in the expression of the oxidative stress marker, nitrotyrosine. Conclusions: Genetic Hmox1 partial deficiency is sufficient to sensitize mice to the development of diabetic glomerular microvascular lesions. HO-1 exerts antioxidant effects in the kidney during diabetes mellitus. These have protective effects on the development of glomerular endothelial injury. |
