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Wen Su

Researcher at Shenzhen University

Publications -  27
Citations -  829

Wen Su is an academic researcher from Shenzhen University. The author has contributed to research in topics: Fatty liver & Nonalcoholic fatty liver disease. The author has an hindex of 13, co-authored 25 publications receiving 560 citations. Previous affiliations of Wen Su include Peking University & University of Houston.

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Comparative proteomic study reveals 17β-HSD13 as a pathogenic protein in nonalcoholic fatty liver disease.

TL;DR: The aim of this study was to determine the function of 17β-hydroxysteroid dehydrogenase-13 (17β-HSD13), one of the authors' newly identified LD-associated proteins in human subjects with normal liver histology and simple steatosis, in NAFLD development.
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FAM3A activates PI3K p110α/Akt signaling to ameliorate hepatic gluconeogenesis and lipogenesis

TL;DR: FAM3A plays crucial roles in the regulation of glucose and lipid metabolism in the liver, where it activates the PI3K‐Akt signaling pathway by way of a Ca2+/CaM‐dependent mechanism.
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Ablation of cytochrome P450 omega-hydroxylase 4A14 gene attenuates hepatic steatosis and fibrosis

TL;DR: It is shown that hepatic CYP4A expression was up-regulated in the livers of patients and three murine models of NAFLD and may represent a potential therapeutic target for the treatment ofNAFLD.
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VSMC-specific EP4 deletion exacerbates angiotensin II-induced aortic dissection by increasing vascular inflammation and blood pressure

TL;DR: It is found that chronic angiotensin II infusion of mice with vascular smooth muscle cell (VSMC)-specific EP4 gene knockout frequently developed aortic dissection (AD) with severe elastic fiber degradation and VSMC dedifferentiation, and EP4 may represent a potential therapeutic target for the treatment of AD.
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Aquaporins in the kidney: physiology and pathophysiology.

TL;DR: This review summarizes current understanding of physiological and pathophysiological roles of AQPs in the kidney, with a focus on recent progress on AQP2 regulation by the nuclear receptor transcriptional factors.