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Xiaoni Kong

Researcher at Shanghai Jiao Tong University

Publications -  64
Citations -  2092

Xiaoni Kong is an academic researcher from Shanghai Jiao Tong University. The author has contributed to research in topics: Medicine & Biology. The author has an hindex of 18, co-authored 40 publications receiving 1529 citations. Previous affiliations of Xiaoni Kong include Shanghai University & National Institutes of Health.

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Interleukin-22 induces hepatic stellate cell senescence and restricts liver fibrosis in mice.

TL;DR: IL‐22 induces the senescence of HSCs, which express both IL‐10R2 and IL‐22R1, thereby ameliorating liver fibrogenesis, in addition to the previously discovered hepatoprotective functions of IL‐ 22.
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Signal Transducer and Activator of Transcription 3 in Liver Diseases: A Novel Therapeutic Target

TL;DR: The cytokines and small molecules that activate STAT3 in hepatocytes may have therapeutic benefits to treat acute liver injury, fatty liver disease, and alcoholic hepatitis, while blockage of STAT3 may have a therapeutic potential to prevent and treat liver cancer.
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The Role of Nrf2 in Liver Disease: Novel Molecular Mechanisms and Therapeutic Approaches.

TL;DR: Recent advances in the function and principal mechanisms by regulating Nrf2 in liver diseases, including acute liver failure, hepatic ischemia–reperfusion injury (IRI), alcoholic liver disease, viral hepatitis, non-alcoholic fatty liver disease (NAFLD), non- alcoholic steatohepatitis (NASH), and hepatocellular carcinoma are discussed.
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Interleukin-22 Promotes Proliferation of Liver Stem/Progenitor Cells in Mice and Patients With Chronic Hepatitis B Virus Infection

TL;DR: In livers of mice and patients with chronic HBV infection, inflammatory cells produce IL-22, which promotes proliferation of LPCs via STAT3, and these findings link inflammation with proliferation ofLPCs in patients withHBV infection.
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Liver is the major source of elevated serum lipocalin‐2 levels after bacterial infection or partial hepatectomy: A critical role for IL‐6/STAT3

TL;DR: Hepatocytes are the major cell type responsible for LCN2 production after bacterial infection or PHx, and this response is dependent on IL‐6 activation of the STAT3 signaling pathway, and plays an important role in inhibiting bacterial infection and promoting liver regeneration.