Yejing Zhu

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The cardiotoxicity of cyclosporine A (CsA) limits its clinical application in extensive and long-term therapies. Our group has shown that CsA induces myocardium cell apoptosis in vivo and increases calcium-sensing receptor (CaSR) expression. However, its molecular mechanism remains unknown. The purpose of this study was to determine whether CaSR plays an(More)
The aim of this study was to investigate whether Cyclosporin-A (CsA)-induced myocardial injury is mediated by elevating the intracellular calcium concentration ([Ca2+]i) through the Calcium sensing receptor (CaSR). Cultured neonatal rat cardiomyocytes were treated with CsA, with or without pretreatment with the CaSR-specific antagonist NPS2390 or the(More)
Cyclosporine (CsA) has become a mainstay for immune suppression of organ transplants. It is known that patients receiving CsA manifest increased growth of aggressive cardiotoxicity. We have demonstrated that CsA induces myocardium cell apoptosis in vivo and vitro. Recently, dishevelled-1 (Dvl-1) protein, which is a cytoplasmic mediator of Wnt/β-catenin(More)
OBJECTIVE In our previous study, we have demonstrated that tissue factor pathway inhibitor (TFPI) gene could induce vascular smooth muscle cell (VSMC) apoptosis. This study was conducted to investigate whether the overexpression of the TFPI gene can induce VSMC apoptosis by inhibiting JAK-2/STAT-3 pathway phosphorylation and thereby inhibiting the(More)
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