作者: Xiaobin Han , Takashi Ito , Junichi Azuma , Stephen W. Schaffer , Russell W. Chesney
DOI: 10.1007/978-3-319-15126-7_19
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摘要: Diabetic nephropathy is the leading cause of end stage renal disease in man. Despite efforts, an ideal animal model that can reproduce characteristics human diabetic has not been developed. To this end, we hypothesize taurine deficiency one critical risk factors for development patients with diabetes mellitus. This hypothesis be tested vivo TauT knockout (TauT −/−) C57BL/6 background mice. We asked whether would enhance streptozotocin-treated mouse. provide evidence alteration gene a substantial effect on susceptibility to kidney −/− mouse diabetes. These animals specifically developed characteristic histological changes included glomerulosclerosis, nodular lesions, arteriosclerosis, arteriolar dilation, and tubulointerstitial fibrosis. Immunohistochemical staining molecular markers such as smooth muscle actin, CD34, Ki67, collagen IV confirmed these observations were abnormal. The results demonstrated deletion predisposes mice develop end-stage disease, which closely replicates pathological features and, thus, serve therapeutic strategies.