Wendong Li
Soochow University (Suzhou)
21 Papers
58 Citations
Wendong Li is an academic researcher from Soochow University (Suzhou). The author has contributed to research in topics: Medicine & Tube formation. The author has an hindex of 11, co-authored 15 publications.
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Papers
EndMT: A promising and controversial field.
TL;DR: EndMT is involved in cardiac development and a variety of diseases processes, such as vascular or tissue fibrosis and tumor, however, its role in specific diseases remains under debate.
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Upregulation of miR-483-3p contributes to endothelial progenitor cells dysfunction in deep vein thrombosis patients via SRF
Lingshang Kong,Nan Hu,Xiaolong Du,Wenbin Wang,Hong Chen,Wendong Li,Sen Wei,Hao Zhuang,Xiao-Qiang Li,Chenglong Li +9 more
TL;DR: miR-483-3p is upregulated in EPCs from DVT patients, and it targets SRF to decrease E PCs migration and tube formation and increase apoptosis in vitro, while decrease EPC's homing and thrombus resolution in vivo.
Metformin inhibits endothelial progenitor cell migration by decreasing matrix metalloproteinases, MMP-2 and MMP-9, via the AMPK/mTOR/autophagy pathway.
TL;DR: The results showed that metformin inhibited the migration of EPCs by decreasing M MP-2 and MMP-9, and the AMPK/mTOR/autophagy pathway was demonstrated to be involved in the regulatory mechanisms.
Downregulation of let-7e-5p contributes to endothelial progenitor cell dysfunction in deep vein thrombosis via targeting FASLG
Lingshang Kong,Xiaolong Du,Nan Hu,Wendong Li,Wenbin Wang,Sen Wei,Hao Zhuang,Xiao-Qiang Li,Chenglong Li +8 more
TL;DR: EPCs overexpressing let-7e-5p exhibited enhanced ability of homing and thrombus revascularization inrat model of venous thrombosis and is a potential therapeutic target in DVT treatment.
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Autophagy inhibits endothelial progenitor cells migration via the regulation of MMP2, MMP9 and uPA under normoxia condition
TL;DR: It is demonstrated that autophagy could regulate the EPCs migration through mTOR-P70 S6K pathway, and MMP2, MMP9 and uPA may also involve in the regulation mechanism.
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