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Shuying Shen on Muck Rack

Shuying Shen

As seen in: Nature, Annals of the Rheumatic Diseases
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Articles

HDAC1 maintains metabolic homeostasis in nucleus pulposus cells via post-translational modification interactions with YBX1

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By Bohao Zhou, Jiechao Xia, Zhaowei Zhang, Bingbing Xu, Zixin Ruan, Fengjie Ma, Zhenlei Zhang, Teng Yao, Jun Gao, Jianle Wang, Zheyuan Zhang, Junxin Chen, Shiyuan Shi, Yongfeng Cui, Panyang Shen, Shuying Shen, Jianjun Ma, Tianyou Gao, Chen’an You
| Nature Verified
Abstract Intervertebral disc degeneration is characterized by the metabolic dysregulation of nucleus pulposus cells, which is regulated by complex post-translational modifications, manifesting as extracellular matrix remodeling and inflammatory microenvironment formation. We demonstrated the progressive downregulation of HDAC1 during disc degeneration. HDAC1 mediates the deacetylation and ubiquitination-dependent degradation of YBX1.
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Chondrocytes reprogram chromatin in hypoxic microenvironments to activate CADM1-AS1/HDAC1 complex-mediated anti-inflammation signals

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By Weiyu Ni, Tianyuan Gu, Panyang Shen, Zixuan Mei, Yizheng Wu, Nan Pan, Wentao Yang, Gang Liu, Yan Ma, Xiangqian Fang, Shunwu Fan, Haitao Zhang, Shuying Shen, Kamuran Yilamu
| Nature Verified
Abstract Maintaining chondrocyte homeostasis is crucial for the effective treatment of osteoarthritis. Chondrocytes reside in a hypoxic environment under physiological conditions. This study, conducted exclusively in male mice, examines the association between epigenetics and chondrocyte homeostasis and observes significant alterations in histone acetylation in chondrocytes under hypoxic conditions.
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Interleukin-16 enhances anti-tumor immune responses by establishing a Th1 cell-macrophage crosstalk through reprogramming glutamine metabolism in mice | Nature Communications

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By tong liu, Yunkun Lu, Junjie Xu, Shuying Shen, Hui Li, Min Shang, Hongshan Guo, Qian Cao, Kai Wang, Wang Qingqing
| Nature Verified
Abstract Overcoming immunosuppression in the tumor microenvironment (TME) is crucial for developing novel cancer immunotherapies. Here, we report that IL-16 administration enhances the polarization of T helper 1 (Th1) cells by inhibiting glutamine catabolism through the downregulation of glutaminase in CD4+ T cells and increases the production of Th1 effector cytokine IFN-γ, thus improving anti-tumor immune responses.
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