Jie Lou
Harbin Medical University
11 Papers
31 Citations
Jie Lou is an academic researcher from Harbin Medical University. The author has contributed to research in topics: Chemistry & Medicine. The author has an hindex of 3, co-authored 7 publications.
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Papers
Homocysteine Causes Endothelial Dysfunction via Inflammatory Factor-Mediated Activation of Epithelial Sodium Channel (ENaC).
Chen Liang,Qiu-Shi Wang,Xu Yang,Di Zhu,Yu Sun,Na Niu,Jie Yao,Bi-Han Dong,Shuai Jiang,Liang-Liang Tang,Jie Lou,Chang-Jiang Yu,Qun Shao,Ming-Ming Wu,Zhi-Ren Zhang +14 more
TL;DR: In this article, the authors investigated whether and how the epithelial sodium channel (ENaC), a recently identified ion channel in endothelial cells, plays a role in hyperhomocysteinemia (HHcy)induced endothelial dysfunction.
AMP-Activated Protein Kinase Attenuates High Salt-Induced Activation of Epithelial Sodium Channels (ENaC) in Human Umbilical Vein Endothelial Cells.
Wei-Wan Zheng,Xin-Yuan Li,Hui-Bin Liu,Zi-Rui Wang,Qing-Qing Hu,Yu-Xia Li,Bin-Lin Song,Jie Lou,Qiu-Shi Wang,He-Ping Ma,Zhi-Ren Zhang +10 more
TL;DR: It is suggested that high sodium stimulates ENaC activation by negatively modulating AMPK activity, thereby leading to reduction in eNOS activity and NO production in endothelial cells.
Inhibition of YAP by lenvatinib in endothelial cells increases blood pressure through ferroptosis.
Chen Liang,Di Zhu,Wei Xia,Zi Hong,Qiu-Shi Wang,Yu Sun,Yan-Chao Yang,Song-Qi Han,Liangiie Tang,Jie Lou,Ming-Ming Wu,Zhi-Ren Zhang +11 more
TL;DR: In this paper , the authors reported that lenvatinib-induced hypertension is associated with ferroptosis of endothelial cells and showed that the inhibition of YAP led to vascular dysfunction and hypertension.
13
TRUSS Exacerbates NAFLD Development by Promoting IκBα Degradation in Mice.
Chang-Jiang Yu,Qiu-Shi Wang,Ming-Ming Wu,Bin-Lin Song,Chen Liang,Jie Lou,Liang-Liang Tang,Xiao-Di Yu,Na Niu,Xu Yang,Bao-Long Zhang,Yao Qu,Yang Liu,Zhi-Chao Dong,Zhi-Ren Zhang +14 more
TL;DR: It is reported that tumor necrosis factor receptor–associated ubiquitous scaffolding and signaling protein (TRUSS) acts as a positive regulator of nonalcoholic fatty liver disease and in a variety of metabolic disorders.
11
Stimulation of Epithelial Sodium Channels in Endothelial Cells by Bone Morphogenetic Protein-4 Contributes to Salt-Sensitive Hypertension in Rats
Xu Yang,Na Niu,Chen Liang,Ming-Ming Wu,Liang-Liang Tang,Qiu-Shi Wang,Jie Lou,Bin-Lin Song,Wei-Wan Zheng,He-Ping Ma,Zhi-Ren Zhang +10 more
TL;DR: Testing a hypothesis that bone morphogenetic protein 4 mediates high salt-induced loss of vascular relaxation by stimulating the epithelial sodium channel in endothelial cells suggests that high salt intake stimulates endothelial Cells to express and release B MP4 and that the released BMP4 reduces artery relaxation by stimulated ENaC in endothelium cells.