awc777万象城娱乐官网附属同济医院消化内科行政副主任

上海市医学会肝病专科分会肝纤维化学组副组长

上海中西医结合学会常务委员

中华医学会消化分会生物样本库与转化医学协作组委员

Liver Research杂志青年编委

Deputy Director, Department of Gastroenterology, Tongji Hospital, School of Medicine, Tongji University

Deputy Team Leader, Liver Fibrosis Group, Liver Disease Branch of Shanghai Medical Association

Executive Committee Member of Shanghai Association of Integrated Traditional Chinese and Western Medicine

Committee member of the Biobank and Translational Medicine Collaboration Group of the Digestive Branch of the Chinese Medical Association

Junior Editorial Board of Liver Research Journal

擅长消化系统各类疾病的诊疗，尤其擅长慢性肝病及其终末期阶段的临床诊疗。入选上海市青年拔尖人才（2020），上海市卫健委“新优青“（2017），上海市卫健委 “医苑新星”（2014），持续致力于慢性肝病与肝纤维化的基础和临床研究，目前在肝病领域主持课题共14项（经费总额400万元），其中包括国家自然科学基金3项，省部级课题4项，以第一/通讯作者在J Hepatol， Adv Sci及Hepatol Int等专业领域国际期刊发表SCI论著16篇，授权专利6 项（含发明3 项）、软著1项。形成的创新成果主要包括三个方面：1) 揭示肝损伤的关键免疫炎症调控机制:①损伤的肝细胞可释放高迁移率组蛋白1(HMGB1),通过诱导自噬，维持调节性T细胞的免疫抑制特性，并可促进肝星状细胞激活、肝纤维化进展，工作发表在Clin Sci (2017, 2018)。②III型固有淋巴细胞、CD161+CD4+T细胞可依赖IL-17信号通路参与肝纤维化进展，工作发表在Clin Sci (2018)及Clin Transl Immunology (2021)；2) 制定肝硬化门脉高压症无创量化临床管理方案：基于三维重建法计算虚拟门静脉压力梯度，构建肝硬化患者首次静脉曲张性出血的无创预警模型，制定临床管理流程，并通过临床探索，证实阻断HMGB1的上游炎症信号——盐皮质激素受体(MR)可降低门静脉压力、延缓疾病进展，工作发表在Hepatol Int (2022)；3) 发现药物性肝损伤 (DILI) 潜在药物干预靶点：选择性激活肝细胞Mas信号，可诱导脂噬及脂肪酸氧化，显著改善DILI，并阐明关键信号通路AKT-FOXO1，工作发表在J Hepatol (2023), 此外髓系Mas是对乙酰氨基酚诱导的DILI微环境中关键的促炎驱动力，数据发表在Adv Sci(2024)。

Specializes in the diagnosis and treatment of various diseases of the digestive system, especially in the clinical management of chronic liver disease and its end-stage. Selected as Shanghai Youth Top Talent (2020), Shanghai Health and Health Commission "New Excellent Youth" (2017), Shanghai Health and Health Commission "New Star in the Medical Park" (2014), focusing on the basic and clinical research of chronic liver disease and liver fibrosis, currently leading a total of 14 projects in the field of liver disease (total funding of 4 million yuan), including 3 projects of the National Natural Science Foundation. 4 provincial and ministerial projects, published 16 Sci papers in international journals in the field of J Hepatol, Adv Sci and Hepatol Int as the first/corresponding author, 6 authorized patents (including 3 inventions), and 1 soft book. The resulting innovation results mainly include three aspects: 1) To reveal the key immunoinflammatory regulatory mechanisms of liver injury: (1) Injured liver cells can release high mobility histone 1(HMGB1), which maintains the immunosuppressive properties of regulatory T cells by inducing autophagy, and can promote the activation of hepatic stellate cells and the progression of liver fibrosis. The work was published in Clin Sci (2017, 2018). (2) Type III intrinsic lymphocytes and CD161+CD4+T cells can participate in the progression of liver fibrosis depending on IL-17 signaling pathway, and the work was published in Clin Sci (2018) and Clin Transl Immunology (2021). 2) Develop non-invasive quantitative clinical management plan for portal hypertension of cirrhosis: The virtual portal pressure gradient was calculated based on 3D reconstruction method to build a non-invasive early warning model for the first varicose hemorrhage in cirrhotic patients, and develop clinical management procedures. Through clinical exploration, it was confirmed that blocking the upstream inflammatory signal of HMGB1, salocorticoid receptor, can reduce portal pressure and delay disease progression. Work is published in Hepatol Int (2022). 3) Potential drug intervention targets for drug-induced liver injury (DILI) were identified: Selective activation of Mas signal in hepatocytes can induce lipophagy and fatty acid oxidation, significantly improve DILI, and elucidate the key signaling pathway AKT-FOXO1, published in the J Hepatol (2023). In addition, myeloid Mas is a key pro-inflammatory driving force in the paracetamen-induced DILI microenvironment. Data were published in Adv Sci(2024).