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Yongzeng Feng

Researcher at Wenzhou Medical College

Publications -  28
Citations -  526

Yongzeng Feng is an academic researcher from Wenzhou Medical College. The author has contributed to research in topics: Wound healing & Angiogenesis. The author has an hindex of 9, co-authored 25 publications receiving 326 citations.

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Metformin protects against apoptosis and senescence in nucleus pulposus cells and ameliorates disc degeneration in vivo.

TL;DR: It is shown that metformin could protect nucleus pulposus cells against apoptosis and senescence via autophagy stimulation and ameliorate disc degeneration in vivo, revealing its potential to be a therapeutic agent for IDD.
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Asperosaponin VI promotes angiogenesis and accelerates wound healing in rats via up-regulating HIF-1α/VEGF signaling.

TL;DR: Asperosaponin VI promotes angiogenesis of HUVECs in vitro via up-regulating the HIF-1α/VEGF pathway, and efficiently enhances the vascularization in regenerated tissue and facilitates wound healing in vivo.
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Monotropein promotes angiogenesis and inhibits oxidative stress-induced autophagy in endothelial progenitor cells to accelerate wound healing

TL;DR: Results showed Mtp promoted mobilization and differentiation of BM‐EPCs and protected against apoptosis and autophagy by suppressing the AMPK/mTOR pathway, improving wound healing in vivo.
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Comparison of percutaneous cannulated screw fixation and calcium sulfate cement grafting versus minimally invasive sinus tarsi approach and plate fixation for displaced intra-articular calcaneal fractures: a prospective randomized controlled trial.

TL;DR: The clinical outcomes are comparable between the two minimally invasive techniques in the treatment of Sanders Type-II DIACFs, and the PR+CSC grafting is superior to the MISTA in terms of the average time between initial injury and operation, operation time, wound-related complications and subtalar joint activity.
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Long non-coding RNA BCAR4 promotes chondrosarcoma cell proliferation and migration through activation of mTOR signaling pathway.

TL;DR: It is found that mTOR overexpression abolished the decrease of chondrosarcoma cell proliferation and migration induced by BCAR4 knockdown, and thus contributed to chondrobarcoma progression.