PTH-induced EndMT via miR-29a-5p/GSAP/Notch1 pathway contributed to valvular calcification in rats with CKD,Cell Proliferation

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PTH-induced EndMT via miR-29a-5p/GSAP/Notch1 pathway contributed to valvular calcification in rats with CKD
Cell Proliferation ( IF 5.9 ) Pub Date : 2021-05-04 , DOI: 10.1111/cpr.13018
Liting Wang _{1,

2} , Rining Tang _{1,

2} , Yuxia Zhang _{1,

2} , Sijie Chen _{1,

2} , Yu Guo _{1,

2} , Xiaochen Wang ₁ , Zixiao Liu ₃ , Hong Liu ₁ , Xiaoliang Zhang ₁ , Bi‐Cheng Liu ₁

Affiliation

Endothelial-to-mesenchymal transition (EndMT) is a common pathophysiology in valvular calcification (VC) among non-chronic kidney disease (CKD) patients. However, few studies were investigated in CKD-induced VC. Parathyroid hormone (PTH) was considered to be an important component of EndMT in CKD-induced cardiovascular diseases. Therefore, determining whether PTH could induce valvular EndMT and elucidating corresponding mechanism involved further study.

中文翻译：

PTH 诱导的 EndMT 通过 miR-29a-5p/GSAP/Notch1 通路导致 CKD 大鼠的瓣膜钙化

内皮-间质转化 (EndMT) 是非慢性肾病 (CKD) 患者瓣膜钙化 (VC) 的常见病理生理。然而，很少有研究在 CKD 诱导的 VC 中进行研究。甲状旁腺激素（PTH）被认为是 CKD 诱发的心血管疾病中 EndMT 的重要组成部分。因此，确定 PTH 是否可以诱导瓣膜 EndMT 并阐明相应的机制需要进一步研究。

更新日期：2021-06-01

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