An Update on the Use of Animal Models in Diabetic Nephropathy Research

被引：65

作者：

Betz, Boris ^{[1
,3
]}

Conway, Bryan R. ^{[2
]}

机构：

[1] Univ Edinburgh, Ctr Inflammat Res, Edinburgh, Midlothian, Scotland

[2] Univ Edinburgh, Queens Med Res Ctr, Ctr Cardiovasc Sci, 47 Little France Crescent, Edinburgh EH16 4TJ, Midlothian, Scotland

[3] Jena Univ Hosp, Dept Clin Chem & Lab Med, Jena, Germany

来源：

CURRENT DIABETES REPORTS | 2016年 / 16卷 / 02期

关键词：

Diabetic nephropathy; Animal models; Hypertension; Transcriptomics; Regression; BLOOD-PRESSURE; ACCELERATED NEPHROPATHY; KIDNEY-DISEASE; MOUSE MODEL; HYPERTENSION; GENE; RAT; PREVENTION; INSULIN; LESIONS;

D O I：

10.1007/s11892-015-0706-2

中图分类号：

R5 [内科学];

学科分类号：

1002 ; 100201 ;

摘要：

In the current review, we discuss limitations and recent advances in animal models of diabetic nephropathy (DN). As in human disease, genetic factors may determine disease severity with the murine FVB and DBA/2J strains being more susceptible to DN than C57BL/6J mice. On the black and tan, brachyuric (BTBR) background, leptin deficient (ob/ob) mice develop many of the pathological features of human DN. Hypertension synergises with hyperglycemia to promote nephropathy in rodents. Moderately hypertensive endothelial nitric oxide synthase (eNOS(-/-)) deficient diabetic mice develop hyaline arteriosclerosis and nodular glomerulosclerosis and induction of renin-dependent hypertension in diabetic Cyp1a1mRen2 rats mimics moderately severe human DN. In addition, diabetic eNOS(-/-) mice and Cyp1a1mRen2 rats recapitulate many of the molecular pathways activated in the human diabetic kidney. However, no model exhibits all the features of human DN; therefore, researchers should consider biochemical, pathological, and transcriptomic data in selecting the most appropriate model to study their molecules and pathways of interest.

引用

页码：1 / 9

页数：9

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