肖武生

助理教授🙇🏻‍♂️、副研究員
wxiao@bjmu.edu.cn
北京海澱區意昂路38號
北

個人簡介

現任意昂体育助理教授🚵、副研究員和博士研究生導師🚝。主要研究環境汙染致心肺血管系統損傷及其分子機理；在Circulation Research, Free Radical Biology and Medicine和Archives of Toxicology等雜誌發表論文17篇；先後參與3項美國NIH和NIEHS資助的科研項目👱‍♀️🫴🏼；擔任Circulation Research，Environmental Health Perspectives和Environmental Pollution等19種期刊的審稿人🤵🏼‍♀️。

主要教育與工作經歷🚶🏻‍♀️：

2022/11- 意昂体育毒理學系助理教授

2021/11-2022/10 哈佛醫意昂和布萊根婦女醫院醫學系講師

2015/01-2021/10 哈佛醫意昂和布萊根婦女醫院醫學系博士後

2010/08-2014/12 愛荷華大學自由基與放射醫學系博士研究生

2007/09-2010/06 復旦大學勞動衛生與毒理學系碩士研究生

2006/08-2007/07 福建省疾病預防控製中心細菌性疾病防治科

2001/09-2006/07 南昌大學意昂体育官网預防醫學學士

主要研究方向

心血管和呼吸系統疾病是危害人群健康的首要疾病👨🏼‍🔧，其發生與危害與環境汙染密切相關🏋🏽‍♀️。本課題組主要圍繞能量代謝和氧化還原穩態兩大機製🫃，探究環境危害暴露如何致心肺血管損傷和如何加劇心肺血管疾病的風險。

課題一：能量代謝與心肺血管損傷和疾病

能量代謝是維持所有生命活動的基礎機製。代謝紊亂參與心肺血管疾病等眾多疾病和不良健康結局的發生與發展。我們致力於研究細胞代謝通路和代謝物水平改變對環境因素（如重金屬、農藥和納米材料等）致心肺血管系統毒性的調控機製和防治。

課題二：氧化還原應激與心肺血管損傷和疾病

氧化還原穩態是由細胞的抗氧化（抗氧化酶和非酶類抗氧化劑）和促氧化體系（氧自由基和氮自由基）共同精細維持🌟🙏。兩大體系失衡將引起氧化應激和還原應激，兩者均可造成細胞功能損傷👋🏼。我們致力於研究環境汙染物暴露如何打破氧化還原體系的平衡，導致心肺血管系統氧化和還原損傷🤕。

代表性科研項目

1. 參與美國NIH R01項目🤵🏻‍♀️：L-2-hydroxyglutarate and metabolic remodeling in hypoxia. 2020-2022

2. 參與美國NIH R37項目😳：GPx-3 and peroxide flux in the endothelial cell. 2015-2017

3. 參與美國NIEHS Superfund項目🧎：Semi-volatile PCB exposure and oxidative stress in mammalian cells. 2010-2014

10篇代表性論文

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.