Xiaoli Sun
Nanjing Medical University
15 Papers
7 Citations
Xiaoli Sun is an academic researcher from Nanjing Medical University. The author has contributed to research in topics: Chemistry & Fibrosis. The author has an hindex of 5, co-authored 8 publications.
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Papers
Wnt/ β -Catenin-Promoted Macrophage Alternative Activation Contributes to Kidney Fibrosis.
Ye Feng,Jiafa Ren,Yuan Gui,Wei Wei,Bingyan Shu,Qingmiao Lu,Xian Xue,Xiaoli Sun,Weichun He,Junwei Yang,Chunsun Dai +10 more
TL;DR: It is shown that activation of Wnt/β-catenin signaling promotes kidney fibrosis by stimulating macrophage M2 polarization and preventing IL-4- or TGFβ1-induced Macrophage alternative (M2) polarization processes.
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Blockade of CD38 diminishes lipopolysaccharide-induced macrophage classical activation and acute kidney injury involving NF-κB signaling suppression.
Bingyan Shu,Ye Feng,Yuan Gui,Qingmiao Lu,Wei Wei,Xian Xue,Xiaoli Sun,Weichun He,Junwei Yang,Chunsun Dai +9 more
TL;DR: It is reported that in cultured macrophages, Lipopolysaccharide (LPS) could upregulate CD38 expression in time and dose dependent manner and CD38 mediates LPS-induced macrophage activation and AKI, which may be treated as a therapeutic target for sepsis-induced AKI in patients.
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Fibroblast mTOR/PPARγ/HGF axis protects against tubular cell death and acute kidney injury.
Yuan Gui,Qingmiao Lu,Mengru Gu,Mingjie Wang,Yan Liang,Xingwen Zhu,Xian Xue,Xiaoli Sun,Weichun He,Junwei Yang,Allan Z. Zhao,Bo Xiao,Chunsun Dai +12 more
TL;DR: The data suggest that mTOR signaling activation in kidney fibroblasts protects against tubular cell death and dictates the outcome of AKI through stimulating PPARγ and HGF expression.
Protein kinase Cα drives fibroblast activation and kidney fibrosis by stimulating autophagic flux
Xian Xue,Jiafa Ren,Jiafa Ren,Xiaoli Sun,Yuan Gui,Ye Feng,Bingyan Shu,Wei Wei,Qingmiao Lu,Yan Liang,Weichun He,Junwei Yang,Chunsun Dai +12 more
TL;DR: It is found that transforming growth factor β1 (TGFβ1) activates PKCα signaling in cultured NRK-49F cells in a time-dependent manner and blocking PKC α activity may retard autophagic flux and thereby prevent fibroblast activation and kidney fibrosis.
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Protein phosphatase 2Acα modulates fatty acid oxidation and glycolysis to determine tubular cell fate and kidney injury.
Mengru Gu,Mengzhu Tan,Lu-Lu Zhou,Xiaoli Sun,Qingmiao Lu,Mingjie Wang,Hanlu Jiang,Yan Liang,Qing Hou,Xian Xue,Zhuo Xu,Chunsun Dai +11 more
TL;DR: In this paper , the authors showed that PP2Acα induction in damaged tubular cells suppresses fatty acid oxidation and promotes glycolysis, leading to cell death and fibrosis.
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