miR-30c Mediates Upregulation of Cdc42 and Pak1 in Diabetic Cardiomyopathy
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چکیده
منابع مشابه
miR-200b Mediates Endothelial-to-Mesenchymal Transition in Diabetic Cardiomyopathy.
Hyperglycemia-induced endothelial injury is a key pathogenetic factor in diabetic cardiomyopathy. Endothelial injury may lead to a phenotypic change (i.e., endothelial-to-mesenchymal transition [EndMT]), causing cardiac fibrosis. Epigenetic mechanisms, through specific microRNA, may regulate such a process. We investigated the mechanisms for such changes in cardiac microvascular endothelial cel...
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Guang Chen, Xing Chen, Aravin Sukumar, Bo Gao, Jessica Curley, H. William Schnaper, Alistair J. Ingram and Joan C. Krepinsky* Division of Nephrology, St. Joseph’s Hospital, McMaster University, Hamilton, ON L8N 4A6, Canada Department of Parasitology, College of Basic Medical Sciences, Jamusi University, Jamusi 154000, China Section of Pediatric Nephrology, University of Chicago, Chicago, IL 606...
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MicroRNAs (miRNAs) play vital roles in the development of diabetic nephropathy. Here, we compared the protective efficacies of miR-26a and miR-30c in renal tubular epithelial cells (NRK-52E) and determined whether they demonstrated additive effects in the attenuation of renal fibrosis. TGFβ1 suppressed miR-26a and miR-30c expression but up-regulated pro-fibrotic markers in NRK-52E cells, and th...
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Epithelial-to-mesenchymal transition (EMT) plays a significant role in tubulointerstitial fibrosis, which is a hallmark of diabetic nephropathy. Thus, identifying the mechanisms of EMT activation could be meaningful. In this study, loss of miR-30c accompanied with increased EMT was observed in renal tubules of db/db mice and cultured HK2 cells exposed to high glucose. To further explore the rol...
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ژورنال
عنوان ژورنال: Cardiovascular Therapeutics
سال: 2015
ISSN: 1755-5914
DOI: 10.1111/1755-5922.12113