miR-21 overexpression enhances TGF-尾1-induced epithelial-to-mesenchymal transition by target smad7 and aggravates renal damage in diabetic nephropathy
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- 作者：Jin-Yang Wanga ; b ; c ; d ; Yan-Bin Gaoa ; c ; gaoyb111@hotmail.com" class="auth_mail ; Na Zhanga ; Da-Wei Zoua ; Peng Wange ; Zhi-Yao Zhua ; Jiao-Yang Lia ; Sheng-Nan Zhoua ; Shao-Cheng Wangb ; Ying-Ying Wangb ; Jin-Kui Yangb ; d ; jinkui.yang@gmail.com" class="auth_mail
- 关键词：EMT ; epithelial-to-mesenchymal transition ; RTIAW ; renal tubular interstitial area width ; CF ; collagen fibers ; V ; vascular ; G ; glomerular ; RTBM ; renal tubular basement membrane ; ACR ; urinary albumin creatinine ratio ; Ccr ; creatinine clearance ratio
- 刊名：Molecular and Cellular Endocrinology
- 出版年：5 July 2014
- 年：2014
- 卷：392
- 期：1-2
- 页码：163-172
- 全文大小：5020 K
文摘
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miR-21 expression was upregulated by TGF-尾1 in time- and concentration-dependent manner.
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miR-21 over-expression enhanced TGF-尾1-induced EMT by directly down-regulating smad7 and indirectly up-regulating smad3.
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miR-21 inhibitor can not only inhibit EMT and fibrosis but also ameliorate renal structure and function.
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Targeting miR-21 may be a better alternative to directly suppress TGF-尾1-mediated fibrosis in DN.