肖武生

助理教授、副研究员
wxiao@bjmu.edu.cn
北京海淀区学院路38号
北

个人简介

现任ju11net九州体育助理教授、副研究员和博士研究生导师。主要研究环境污染致心肺血管系统损伤及其分子机理；在Circulation Research, Free Radical Biology and Medicine和Archives of Toxicology等杂志发表论文17篇；先后参与3项美国NIH和NIEHS资助的科研项目；担任Circulation Research，Environmental Health Perspectives和Environmental Pollution等19种期刊的审稿人。

主要教育与工作经历：

2022/11- ju11net九州体育毒理学系助理教授

2021/11-2022/10 哈佛医学院和布莱根妇女医院医学系讲师

2015/01-2021/10 哈佛医学院和布莱根妇女医院医学系博士后

2010/08-2014/12 爱荷华大学自由基与放射医学系博士研究生

2007/09-2010/06 复旦大学劳动卫生与毒理学系硕士研究生

2006/08-2007/07 福建省疾病预防控制中心细菌性疾病防治科

2001/09-2006/07 南昌大学公共卫生学院预防医学学士

主要研究方向

心血管和呼吸系统疾病是危害人群健康的首要疾病，其发生与危害与环境污染密切相关。本课题组主要围绕能量代谢和氧化还原稳态两大机制，探究环境危害暴露如何致心肺血管损伤和如何加剧心肺血管疾病的风险。

课题一：能量代谢与心肺血管损伤和疾病

能量代谢是维持所有生命活动的基础机制。代谢紊乱参与心肺血管疾病等众多疾病和不良健康结局的发生与发展。我们致力于研究细胞代谢通路和代谢物水平改变对环境因素（如重金属、农药和纳米材料等）致心肺血管系统毒性的调控机制和防治。

课题二：氧化还原应激与心肺血管损伤和疾病

氧化还原稳态是由细胞的抗氧化（抗氧化酶和非酶类抗氧化剂）和促氧化体系（氧自由基和氮自由基）共同精细维持。两大体系失衡将引起氧化应激和还原应激，两者均可造成细胞功能损伤。我们致力于研究环境污染物暴露如何打破氧化还原体系的平衡，导致心肺血管系统氧化和还原损伤。

代表性科研项目

1. 参与美国NIH R01项目：L-2-hydroxyglutarate and metabolic remodeling in hypoxia. 2020-2022

2. 参与美国NIH R37项目：GPx-3 and peroxide flux in the endothelial cell. 2015-2017

3. 参与美国NIEHS Superfund项目：Semi-volatile PCB exposure and oxidative stress in mammalian cells. 2010-2014

10篇代表性论文

1. He H, Mulhern RM, Oldham WM, Xiao W, Lin Y, Liao R, Loscalzo J. L-2-hydroxyglutarate protects against cardiac injury via metabolic remodeling. Circulation Research. 2022, 131: 562-579.

2. Xiao W, Oldham WM, Priolo C, Pandey AK, Loscalzo J. Immunometabolic endothelial phenotypes: integrating inflammation and glucose metabolism. Circulation Research. 2021, 129: 9-29.

3. Xiao W and Loscalzo J. Metabolic response to reductive stress. Antioxidants & Redox Signaling. 2020, 32: 1330-1347.

4. Xiao W, Wang RS, Handy DE, Loscalzo J. NAD(H) and NADP(H) redox couples and cellular energy metabolism. Antioxidants & Redox Signaling. 2018, 28: 251-272.

5. Xiao W, Sarsour EH, Wagner BA, Doskey CM., Buettner GR, Domann FE, Goswami PC. Succinate dehydrogenase activity regulates PCB3-quinone induced metabolic oxidative stress and toxicity in HaCaT human keratinocytes. Archives of Toxicology. 2016, 90: 319-332.

6. Xiao W, Vorrink SU, Domann FE, Goswami PC. Ligand-independent activation of aryl hydrocarbon receptor signaling in PCB3-quinone treated HaCaT human keratinocytes. Toxicology Letters. 2015, 233: 258-266.

7. Xiao W and Goswami PC. Down-regulation of peroxisome proliferator activated receptor γ coactivator 1α induces oxidative stress and toxicity of 1-(4-Chlorophenyl)-benzo-2,5-quinone in HaCaT human keratinocytes. Toxicology In Vitro. 2015, 29: 1332-1338.

8. Xiao W, Zhu Y, Sarsour EH, Kalen AL, Aykin-Burns N, Spitz DR, Goswami PC. Selenoprotein P regulates 1-(4-Chlorophenyl)-benzo-2,5-quinone induced oxidative stress and toxicity in human keratinocytes. Free Radical Biology and Medicine. 2013, 65: 70-77.

9. Xiao W, Zhang J, Liang J, Zhu H, Zhou Z, Wu Q. Adverse effects of neonatal exposure 3,3',4,4',5,5'-hexachlorobiphenyl on hormone levels and testicular function in male Sprague-Dawley rats. Environmental Toxicology. 2011, 26: 657-668.

10. Xiao W, Li K, Wu Q, Nishimura N, Chang X, Zhou Z. Influence of persistent thyroxine reduction on spermatogenesis in rats neonatally exposed to 2,2',4,4',5,5'-hexachlorobiphenyl. Birth Defects Research. 2010, 89: 18-25.