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  • 万军 心内
    教学指导委员会副主任、心血管病研究所副所长、主任医师、教授、博士生导师、长江学者
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    导师介绍

    姓名 万军
    出生年月 1963年1月
    单位 武汉大学人民医院心血管内科
    所属学科 临床医学-内科学
    职务、职称及头衔 教学指导委员会副主任、心血管病研究所副所长、主任医师、教授、博士生导师、长江学者
    E-mail wanjun@whu.edu.cn
    联系方式 13907126516
    研究方向 1. 炎症反应与心血管疾病:从炎症发生和炎症消退两个角度,系统研究不同炎症介质、促炎症消退脂质分子及其受体及不同免疫细胞在心血管疾病中的作用及其机制,为心血管疾病的预防和治疗提供新靶点。
    2. 人工智能与互联网+医疗应用:探索人工智能与主动健康相结合在慢病管理领域的应用,致力于推动“互联网+”新型医疗服务模式。
    3. 医疗器械监管科学:聚焦创新医疗器械研发与监管新方法、新标准、新技术研究。
    个人简介 主要从事心血管疾病的诊断和治疗工作,聚焦免疫炎症机制在心血管疾病的研究,在该领域以通讯作者身份在Hypertension、Cardiovascular Research、Journal of the American Heart Association、EBioMedicine等杂志上发表SCI期刊收录文章七十余篇。主持科研项目10项,其中国家自然科学基金3项,湖北省自然科学基金4项,其他项目4项。已培养硕士生18名,博士生8名。目前正在培养的博士生7名,硕士生8名。
    学术任职与荣誉 中华医学会心血管病分会急重症学组委员
    国家医疗保障局DRG付费专家组成员
    湖北省心血管病防治中心高血压达标中心主任
    中华医学会武汉市心血管分会第十九届副主任委员
    湖北省急性心血管病救治中心专家委员会副主任委员
    湖北省医院协会第三届理事会副会长
    湖北省医学会第二十三届理事会副会长
    国家药品监督管理局医疗器械监管科学研究基地(武汉大学)执行主任
    国家卫生健康委药事管理与药物治疗学委员会委员
    国家药品监督管理局第二届医疗器械分类技术委员会执行委员会委员
    中国药品监督管理研究会监管科学研究分会副会长
    教育履历 1980.09-1985.06咸宁医学院临床医学专业本科生获学士学位
    1988.09-1991.06湖北医科大学(现武汉大学第一临床学院)内科学硕士研究生获硕士学位
    1999.09-2002.06武汉大学第一临床学院内科学博士研究生获博士学位
    工作履历 1985.07-1988.09 咸宁医学院助教
    1991.07-1999.09 武汉市第五医院,心内科,主治医师、副主任医师
    2002.07-至今   武汉大学人民医院心血管内科主任医师、教授
    2012.12-2021.12 武汉大学人民医院副院长
    2020.02-2020.03 武昌方舱医院院长
    2022.01-至今   武汉大学人民医院教学指导委员会副主任,兼任心血管病研究所副所长
    成果获奖 1.《基于人工智能的“主动120”新型健康保健与急危重症救治服务模式研究》2018年获第二十届中国国际高新技术成果交易会“优秀产品奖”
    2. 2020年被评为“全国卫生健康系统新冠肺炎疫情防控工作先进个人”
    3.《高血压及其合并症的免疫机制与防治策略创新》以第一完成人获得2022年湖北省科技进步奖二等奖
    代表性论著 1、高血压与血管重构
    (1)Pan W, Zhang J, Wang M, Ye J, Xu Y, Shen B, He H, Wang Z, Ye D, Zhao M, Luo Z, Liu M, Zhang P, Gu J, Liu M, Li D, Liu J, Wan J*, Clinical Features of COVID-19 in Patients With Essential Hypertension and the Impacts of Renin-angiotensin-aldosterone System Inhibitors on the Prognosis of COVID-19 Patients, Hypertension. 2020; 76(3):732-741.
    (2)Zhang J, Liu J, Zhao M, Ye J, Xu Y, Wang Z, Ye D, Ding W, Li D, Liu M, Wang M*, Wan J*. The expression of interleukin 20 increases in plasma and aortic tissues from patients with acute aortic dissection. Clin Chim Acta. 2020;510:373-380. doi: 10.1016/j.cca.2020.07.049.
    (3)Ye J, Wang Y, Wang Z, Liu L, Yang Z, Wang M, Xu Y, Ye D, Zhang J, Zhou Q, Lin Y*, Ji Q*, Wan J*. The Expression of IL-12 Family Members in Patients with Hypertension and Its Association with the Occurrence of Carotid Atherosclerosis. MEDIAT INFLAMM. 2020; 2020 2369279. doi: 10.1155/2020/2369279
    (4)Ye J, Que B, Huang Y, Lin Y, Chen J, Liu L, Shi Y, Wang Y, Wang M, Zeng T, Wang Z, Hu H, Xu Y, Shi L, Ye D, Liu J, Jiang H, Wan J*, Ji Q*. Interleukin-12p35 knockout promotes macrophage differentiation, aggravates vascular dysfunction and elevates blood pressure in angiotensin II-infused mice. Cardiovasc Res. 2019; 115(6): 1102-1113
    (5)Jiang H, Wang M, Ye J, Liu J, Wang Z, Xu Y, Ye D, Wan J*. Serum Levels of Complement-C1q/Tumor Necrosis Factor-Related Protein-3 Decreased in Patients With Acute Aortic Dissection. AM J CARDIOL. 2018; 122 (7): 1244-1248. doi: 10.1016/j.amjcard.2018.06.024
    (6)Ye J, Wang Y, Wang Z, Ji Q, Huang Y, Zeng T, Hu H, Ye D, Wan J*, Lin Y*. Circulating Th1, Th2, Th9, Th17, Th22, and Treg Levels in Aortic Dissection Patients. MEDIAT INFLAMM. 2018; 2018 5697149. doi: 10.1155/2018/5697149
    (7)Ye J, Ji Q, Liu J, Liu L, Huang Y, Shi Y, Shi L, Wang M, Liu M, Feng Y, Jiang H, Xu Y, Wang Z, Song J, Lin Y*, Wan J*. Interleukin 22 promotes blood pressure elevation and endothelial dysfunction in angiotensin II-treated mice. J Am Heart Assoc. 2017; 6(10):e005875. doi: 10.1161/JAHA.117.005875.
    (8)Ye, J; Wang, M; Jiang, H; Ji, Q; Huang, Ying; Liu, J; Zeng, Tao; Xu, Y; Wang, Z; Lin, Y*; Wan, J*. Increased levels of interleukin-22 in thoracic aorta and plasma from patients with acute thoracic aortic dissection. CLIN CHIM ACTA. 2017; 486 395-401. doi: 10.1016/j.cca.2017.10.033
    2、心肌损伤与心肌重构
    (1)Wang M, Zhang J, Yin Z, Ding W, Zhao M, Liu J, Xu Y, Xu S, Pan W, Wei C, Jiang H*, Wan J*. Microglia-Mediated Neuroimmune Response Regulates Cardiac Remodeling After Myocardial Infarction. J Am Heart Assoc. 2023;12(12):e029053. doi: 10.1161/JAHA.122.029053.
    (2)Wang M, Zhao M, Xu S, Zheng Z, Zhang J, Pan W, Yin Z, Liu J, Wei C, Wan J*, Xu Y*. TRPA1 deficiency attenuates cardiac fibrosis via regulating GRK5/NFAT signaling in diabetic rats. Biochem Pharmacol. 2023;214:115671.
    (3)Wang M, Zhao M, Zheng Z, Pan W, Zhang J, Yin Z, Wei C, Xu Y*, Wan J*. TRPA1 deficiency aggravates dilated cardiomyopathy by promoting S100A8 expression to induce M1 macrophage polarization in rats. FASEB J. 2023;37(6):e22982. doi: 10.1096/fj.202202079RR.
    (4)Feng Y, Ji Q, Ye D, Pan H, Lu X, Gan L, Wang M, Liu J, Xu Y, Zhang J, Zhao M, Xu S, Yin Z, Pan W, Wei C, Liu M, Wan J*, Ye J*. IL-27p28 knockout aggravates Doxorubicin-induced cardiotoxicity by regulating Macrophage polarization. Biochem Pharmacol. 2023;210:115469. doi: 10.1016/j.bcp.2023.115469.
    (5)Wang M, Zhang J, Zhao M, Liu J, Ye J, Xu Y, Wang Z, Ye D, Li D, Wan J*. Resolvin D1 Attenuates Doxorubicin-Induced Cardiotoxicity by Inhibiting Inflammation, Oxidative and Endoplasmic Reticulum Stress. Front Pharmacol. 2022;12:749899. doi: 10.3389/fphar.2021.749899
    (6)Wang Z, Liu M, Ye D, Ye J, Wang M, Liu J, Xu Y, Zhang J, Zhao M, Feng Y, Xu S, Pan W, Luo Z, Li D, Wan J*. Il12a Deletion Aggravates Sepsis-Induced Cardiac Dysfunction by Regulating Macrophage Polarization. Front Pharmacol. 2021;12:632912. doi: 10.3389/fphar.2021.632912.
    (7)Ye, J; Wang, Y; Xu, Y; Wang, Z; Liu, L; Wang, M; Ye, D; Zhang, J; Yang, Z; Lin, Y*; Ji, Q*; Wan, J*. Interleukin-22 deficiency alleviates doxorubicin-induced oxidative stress and cardiac injury via the p38 MAPK/macrophage/Fizz3 axis in mice. Redox Biol. 2020; 36 101636. doi: 10.1016/j.redox.2020.101636
    (8)Zhang J, Wang M, Ding W, Zhao M, Ye J, Xu Y, Wang Z, Ye D, Li D, Liu J, Wan J*. Resolvin E1 protects against doxorubicin-induced cardiotoxicity by inhibiting oxidative stress, autophagy and apoptosis by targeting AKT/mTOR signaling. Biochem Pharmacol. 2020;180:114188. doi: 10.1016/j.bcp.2020.114188
    (9)Zhang J, Wang M, Ye J, Liu J, Xu Y, Wang Z, Ye D, Zhao M, Wan J*. The anti-inflammatory mediator Resolvin E1 protects mice against LPS-induced heart injury. Front Pharmacol. 2020;11:203. doi: 10.3389/fphar.2020.00203.
    (10)Wang M, Liu M, Zhang J, Liu J, Ye J, Xu Y, Wang Z, Ye D, Zhao M, Wan J*. Resolvin D1 protects against sepsis-induced cardiac injury in mice. Biofactors. 2020;46(5):766-776. doi: 10.1002/biof.1668.
    (11)Ye J, Huang Y, Que B, Chang C, Liu W, Hu H, Liu L, Shi Y, Wang Y, Wang M, Zeng T, Zhen W, Xu Y, Shi L, Liu J, Jiang H, Ye D, Lin Y *, Wan J*, Ji Q *. Interleukin-12p35 knock out aggravates doxorubicin-induced cardiac injury and dysfunction by aggravating the inflammatory response, oxidative stress, apoptosis and autophagy in mice. EBioMedicine. 2018; 35: 29-39.
    (12)Wang Z, Xu Y, Wang M, Ye J, Liu J, Jiang H, Ye D, Wan J*. TRPA1 inhibition ameliorates pressure overload-induced cardiac hypertrophy and fibrosis in mice. EBioMedicine. 2018; 36: 54-62.
    Name Jun Wan
    Date of birth January,1963
    Department Department of Cardiology, Renmin Hospital, Wuhan University 
    Title Deputy Director of the Teaching Steering Committee,Deputy Director of the Institute of Cardiovascular Diseases,Chief physician,Professor, Doctoral tutor,The Yangtze River Scholar
    Email wanjun@whu.edu.cn
    TEL 13907126516
    Research Direction 1. Inflammation and cardiovascular diseases. Our research is mainly focused on the potential roles and underlying mechanisms of inflammatory mediators such as interleukins and inflammatory cells such as macrophages during the development of cardiovascular diseases. These work will provide therapeutic targets for cardiovascular diseases.
    2. AI and Internet plus medical applications. In recent years, he has explored the application of artificial intelligence and active health in the field of slow disease management, and is committed to building big data platform and promoting internet medical mode.
    3. Medical Device Regulation Science. He has been focused on innovative research and development of medical devices, as well as research on new methods, standards, and technologies for regulation.
    Personal Profile He is mainly engaged in the diagnosis and treatment of cardiovascular diseases, and has presided 10 scientific research projects, including 3 items from the National Natural Science Foundation, 4 items from the Hubei provincial Science and Technology Department.Besides, there are more than 50 articles published in peer-reviewed journals, including Hypertension, Cardiovascular Research, JAHA, Ebiomedicine. By now, he has educated 18 masters and 8 doctor students. At present, there are 7 doctors and 8 masters studying with him.
    Selected Publications  1、Hypertension and Vascular Remodeling
    (1)Pan W, Zhang J, Wang M, Ye J, Xu Y, Shen B, He H, Wang Z, Ye D, Zhao M, Luo Z, Liu M, Zhang P, Gu J, Liu M, Li D, Liu J, Wan J*, Clinical Features of COVID-19 in Patients With Essential Hypertension and the Impacts of Renin-angiotensin-aldosterone System Inhibitors on the Prognosis of COVID-19 Patients, Hypertension. 2020; 76(3):732-741.
    (2)Zhang J, Liu J, Zhao M, Ye J, Xu Y, Wang Z, Ye D, Ding W, Li D, Liu M, Wang M*, Wan J*. The expression of interleukin 20 increases in plasma and aortic tissues from patients with acute aortic dissection. Clin Chim Acta. 2020;510:373-380. doi: 10.1016/j.cca.2020.07.049.
    (3)Ye J, Wang Y, Wang Z, Liu L, Yang Z, Wang M, Xu Y, Ye D, Zhang J, Zhou Q, Lin Y*, Ji Q*, Wan J*. The Expression of IL-12 Family Members in Patients with Hypertension and Its Association with the Occurrence of Carotid Atherosclerosis. MEDIAT INFLAMM. 2020; 2020 2369279. doi: 10.1155/2020/2369279
    (4)Ye J, Que B, Huang Y, Lin Y, Chen J, Liu L, Shi Y, Wang Y, Wang M, Zeng T, Wang Z, Hu H, Xu Y, Shi L, Ye D, Liu J, Jiang H, Wan J*, Ji Q*. Interleukin-12p35 knockout promotes macrophage differentiation, aggravates vascular dysfunction and elevates blood pressure in angiotensin II-infused mice. Cardiovasc Res. 2019; 115(6): 1102-1113
    (5)Jiang H, Wang M, Ye J, Liu J, Wang Z, Xu Y, Ye D, Wan J*. Serum Levels of Complement-C1q/Tumor Necrosis Factor-Related Protein-3 Decreased in Patients With Acute Aortic Dissection. AM J CARDIOL. 2018; 122 (7): 1244-1248. doi: 10.1016/j.amjcard.2018.06.024
    (6)Ye J, Wang Y, Wang Z, Ji Q, Huang Y, Zeng T, Hu H, Ye D, Wan J*, Lin Y*. Circulating Th1, Th2, Th9, Th17, Th22, and Treg Levels in Aortic Dissection Patients. MEDIAT INFLAMM. 2018; 2018 5697149. doi: 10.1155/2018/5697149
    (7)Ye J, Ji Q, Liu J, Liu L, Huang Y, Shi Y, Shi L, Wang M, Liu M, Feng Y, Jiang H, Xu Y, Wang Z, Song J, Lin Y*, Wan J*. Interleukin 22 promotes blood pressure elevation and endothelial dysfunction in angiotensin II-treated mice. J Am Heart Assoc. 2017; 6(10):e005875. doi: 10.1161/JAHA.117.005875.
    (8)Ye, J; Wang, M; Jiang, H; Ji, Q; Huang, Ying; Liu, J; Zeng, Tao; Xu, Y; Wang, Z; Lin, Y*; Wan, J*. Increased levels of interleukin-22 in thoracic aorta and plasma from patients with acute thoracic aortic dissection. CLIN CHIM ACTA. 2017; 486 395-401. doi: 10.1016/j.cca.2017.10.033
    2、Myocardial injury and myocardial remodeling
    (1)Wang M, Zhang J, Yin Z, Ding W, Zhao M, Liu J, Xu Y, Xu S, Pan W, Wei C, Jiang H*, Wan J*. Microglia-Mediated Neuroimmune Response Regulates Cardiac Remodeling After Myocardial Infarction. J Am Heart Assoc. 2023;12(12):e029053. doi: 10.1161/JAHA.122.029053.
    (2)Wang M, Zhao M, Xu S, Zheng Z, Zhang J, Pan W, Yin Z, Liu J, Wei C, Wan J*, Xu Y*. TRPA1 deficiency attenuates cardiac fibrosis via regulating GRK5/NFAT signaling in diabetic rats. Biochem Pharmacol. 2023;214:115671.
    (3)Wang M, Zhao M, Zheng Z, Pan W, Zhang J, Yin Z, Wei C, Xu Y*, Wan J*. TRPA1 deficiency aggravates dilated cardiomyopathy by promoting S100A8 expression to induce M1 macrophage polarization in rats. FASEB J. 2023;37(6):e22982. doi: 10.1096/fj.202202079RR.
    (4)Feng Y, Ji Q, Ye D, Pan H, Lu X, Gan L, Wang M, Liu J, Xu Y, Zhang J, Zhao M, Xu S, Yin Z, Pan W, Wei C, Liu M, Wan J*, Ye J*. IL-27p28 knockout aggravates Doxorubicin-induced cardiotoxicity by regulating Macrophage polarization. Biochem Pharmacol. 2023;210:115469. doi: 10.1016/j.bcp.2023.115469.
    (5)Wang M, Zhang J, Zhao M, Liu J, Ye J, Xu Y, Wang Z, Ye D, Li D, Wan J*. Resolvin D1 Attenuates Doxorubicin-Induced Cardiotoxicity by Inhibiting Inflammation, Oxidative and Endoplasmic Reticulum Stress. Front Pharmacol. 2022;12:749899. doi: 10.3389/fphar.2021.749899
    (6)Wang Z, Liu M, Ye D, Ye J, Wang M, Liu J, Xu Y, Zhang J, Zhao M, Feng Y, Xu S, Pan W, Luo Z, Li D, Wan J*. Il12a Deletion Aggravates Sepsis-Induced Cardiac Dysfunction by Regulating Macrophage Polarization. Front Pharmacol. 2021;12:632912. doi: 10.3389/fphar.2021.632912.
    (7)Ye, J; Wang, Y; Xu, Y; Wang, Z; Liu, L; Wang, M; Ye, D; Zhang, J; Yang, Z; Lin, Y*; Ji, Q*; Wan, J*. Interleukin-22 deficiency alleviates doxorubicin-induced oxidative stress and cardiac injury via the p38 MAPK/macrophage/Fizz3 axis in mice. Redox Biol. 2020; 36 101636. doi: 10.1016/j.redox.2020.101636
    (8)Zhang J, Wang M, Ding W, Zhao M, Ye J, Xu Y, Wang Z, Ye D, Li D, Liu J, Wan J*. Resolvin E1 protects against doxorubicin-induced cardiotoxicity by inhibiting oxidative stress, autophagy and apoptosis by targeting AKT/mTOR signaling. Biochem Pharmacol. 2020;180:114188. doi: 10.1016/j.bcp.2020.114188
    (9)Zhang J, Wang M, Ye J, Liu J, Xu Y, Wang Z, Ye D, Zhao M, Wan J*. The anti-inflammatory mediator Resolvin E1 protects mice against LPS-induced heart injury. Front Pharmacol. 2020;11:203. doi: 10.3389/fphar.2020.00203.
    (10)Wang M, Liu M, Zhang J, Liu J, Ye J, Xu Y, Wang Z, Ye D, Zhao M, Wan J*. Resolvin D1 protects against sepsis-induced cardiac injury in mice. Biofactors. 2020;46(5):766-776. doi: 10.1002/biof.1668.
    (11)Ye J, Huang Y, Que B, Chang C, Liu W, Hu H, Liu L, Shi Y, Wang Y, Wang M, Zeng T, Zhen W, Xu Y, Shi L, Liu J, Jiang H, Ye D, Lin Y *, Wan J*, Ji Q *. Interleukin-12p35 knock out aggravates doxorubicin-induced cardiac injury and dysfunction by aggravating the inflammatory response, oxidative stress, apoptosis and autophagy in mice. EBioMedicine. 2018; 35: 29-39.
    (12)Wang Z, Xu Y, Wang M, Ye J, Liu J, Jiang H, Ye D, Wan J*. TRPA1 inhibition ameliorates pressure overload-induced cardiac hypertrophy and fibrosis in mice. EBioMedicine. 2018; 36: 54-62.