Xu Yang
Harbin Medical University
10 Papers
22 Citations
Xu Yang is an academic researcher from Harbin Medical University. The author has contributed to research in topics: Epithelial sodium channel & SGK1. The author has an hindex of 4, co-authored 9 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.
Oxidized low-density lipoprotein stimulates epithelial sodium channels in endothelial cells of mouse thoracic aorta.
Chen Liang,Qiu-Shi Wang,Xu Yang,Na Niu,Qing-Qing Hu,Bao-Long Zhang,Ming-Ming Wu,Chang-Jiang Yu,Xiao Chen,Bin-Lin Song,Zhi-Ren Zhang,He-Ping Ma +11 more
TL;DR: The epithelial sodium channel (ENaC) is expressed in endothelial cells and acts as a negative modulator of vasodilatation and its associated signal transduction pathway is examined.
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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.
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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.
Endothelial epithelial sodium channel involves in high-fat diet-induced atherosclerosis in low-density lipoprotein receptor-deficient mice.
Na Niu,Xu Yang,Bao-Long Zhang,Chen Liang,Di Zhu,Qiu-Shi Wang,Yong-Xu Cai,Yan-Chao Yang,Xue Ao,Ming-Ming Wu,Zhi-Ren Zhang +10 more
TL;DR: HFD- induced activation of ENaC stimulates inflammatory signaling, thereby contributes to HFD-induced endothelial dysfunction and atherosclerotic lesion formation, and targeting endothelial ENac may be a promising strategy to halt atherogenesis.
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