S
Sheng Chen
Researcher at Huazhong University of Science and Technology
Publications - 15
Citations - 358
Sheng Chen is an academic researcher from Huazhong University of Science and Technology. The author has contributed to research in topics: Autophagy & Viability assay. The author has an hindex of 8, co-authored 15 publications receiving 180 citations.
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Journal ArticleDOI
TGF-β signaling in intervertebral disc health and disease.
TL;DR: Investigation of the changing role of TGF-β signaling in IVD at different pathophysiological stages and its specific molecular mechanisms are needed will contribute to safe and effective TGF -β signaling-based treatments for IVD degeneration.
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HIF1A Alleviates compression-induced apoptosis of nucleus pulposus derived stem cells via upregulating autophagy
He Ruijun,He Ruijun,Zhe Wang,Min Cui,Sheng Liu,Wei Wu,Chen Mo,Yongchao Wu,Yanji Qu,Hui Lin,Sheng Chen,Baichuan Wang,Zengwu Shao +12 more
TL;DR: In this article, the authors studied the effect of hypoxia inducible factor 1 subunit alpha (HIF1A) on intervertebral disc degeneration in both rats and humans.
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Mesenchymal Stem Cells Protect Nucleus Pulposus Cells from Compression-Induced Apoptosis by Inhibiting the Mitochondrial Pathway
TL;DR: It is suggested that BMSCs can protect against compression-induced apoptosis of NPCs by inhibiting the mitochondrial pathway and thus enhance the understanding on the MSC-based therapy for IVDD.
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Hydrogen peroxide induces programmed necrosis in rat nucleus pulposus cells through the RIP1/RIP3-PARP-AIF pathway.
Lei Zhao,Hui Lin,Songfeng Chen,Sheng Chen,Min Cui,Deyao Shi,Baichuan Wang,Kaige Ma,Zengwu Shao +8 more
TL;DR: Under oxidative stress, RIP1/RIP3‐mediated programmed necrosis, executed through the PARP‐AIF pathway, played an important role in NP cell death, and Protective strategies aiming to regulate programmed Necrostatin‐1 may exert a beneficial effect for NP cells survival, and ultimately retard intervertebral disc degeneration.
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TIGAR impedes compression‐induced intervertebral disc degeneration by suppressing nucleus pulposus cell apoptosis and autophagy
TL;DR: TIGAR acted as an important endogenous negative regulator of ROS levels, which might inhibit compression‐induced apoptosis and autophagy through SP1‐dependent mechanisms, and established that mithramycin A could inhibit TIGAR expression and Autophagy levels in NP cells under compression conditions, while PFTα had no similar effect.