Office: 359 Linus Pauling Science Center
Telephone: (541) 737-5081
Fax: (541) 737-5077
Email Address: firstname.lastname@example.org
Mailing/Express Delivery Address:
Weijian Zhang, Ph.D.
Linus Pauling Institute
Oregon State University
307 Linus Pauling Science Center
Corvallis, OR 97331
Compelling evidence links oxidative stress and inflammation to major cardiovascular diseases (CVD), including atherosclerosis, hypertension, coronary heart disease, and stroke. While antioxidants and anti-inflammatories have been found to inhibit atherosclerosis in experimental animals, antioxidant vitamin trials to prevent or slow CVD in humans have been disappointing. The disparity between clinical trials and animal studies points to major gaps in our understanding of the effects and mechanisms of antioxidants in atherosclerotic vascular diseases in humans. Our long-term goal is to target oxidative stress and inflammation in humans to better understand their etiologic roles in atherosclerosis. The intracellular redox environment regulates endothelial cell function; an imbalance in this redox environment may cause upregulation of cellular adhesion molecules and pro-inflammatory and prothrombotic mediators, all of which promote atherosclerosis. We have found that lipoic acid affects redox-sensitive cellsignaling processes, transcription factors, and gene expression in endothelial and mononuclear cells, and exerts strong anti-inflammatory and anti-atherogenic effects in experimental animals. In collaboration with researchers at Oregon Health & Science University, we are currently testing whether lipoic acid supplementation reduces risk factors for the development of atherosclerosis in humans by attenuating oxidative stress and inflammation.
|1982||M.D., Jishou University School of Medicine, P.R. China|
|1987||M.S., Beijing University of Chinese Medicine & Pharmacology (BUCMP), P. R. China|
|1996||Ph.D., Institute of Vascular Biology and Thrombosis Research, University of Vienna, Austria|
|1982-1984||Resident Physician, Dept. of Internal Medicine, Changsha No. 1. Hospital, China|
|1987-1988||Assistant of Physiology, Dept. of Physiology, BUCMP, China|
|1988-1992||Lecturer of Physiology, Dept. of Physiology, BUCMP, China|
|1996||Postdoctoral Fellow, Institute of Vascular Biology and Thrombosis Research, University of Vienna, Austria|
|1996-1997||Faculty Research Associate, Division of Cell Biology, The Hospital for Sick Children, the Dept. of Surgery, Toronto Hospital, University of Toronto, Canada|
|1997-1998||Faculty Research Associate, Institute for Gene Therapy and Molecular Medicine, The Mount Sinai Medical Center, The Mount Sinai School of Medicine, New York University, USA|
|1998-2001||Faculty Research Associate, Linus Pauling Institute, Oregon State University, USA|
|2002-2011||Assistant Professor (Sr. Res.), Linus Pauling Institute, Oregon State University|
|2009-2011||Assistant Professor (Sr. Res.), Department of Biochemistry and Biophysics, College of Science, Oregon State University|
|2011-present||Associate Professor (Sr. Res.), Linus Pauling Institute, and Department of Biochemistry and Biophysics, College of Science, Oregon State University|
|1987||Second prize of “Excellent Scientific Research Paper”, Beijing Association of the Integration of Traditional and Western Medicine, Beijing, China|
|1988||Third prize of “Sun's Foundation for Medical Science Development”, The Ministry of Health, Beijing, China|
|1988-1990||Prize of “Excellent Scientific Research Papers”, BUCMP, Beijing, China|
|1992-1995||North-South Dialogue Scholarship (EH-project 894), the Austrian Academic Exchange Service, the Ministry of Education, Vienna, Austria|
|1994||First prize of "Highest Rated Abstract", 38th Annual Meeting of the German Society for Thrombosis and Hemostasis Research, Munich, Germany|
|1994||First prize of "Erwin Deutsch-Poster Award", Update in Thrombolysis Conference, Vienna, Austria|
|1998-present||Member of the American Association for the Advancement of Science|
|2000-present||Member of the American Heart Association|
|1998-2000||NIH R01 HL56170 (Co-investigator, project 1)|
|2000-2005||NIH P01 HL60886 (Co-investigator, project 1)|
|2001-2003||NIH R03 ES11542 (Principal Investigator)|
|2002-2003||Pilot Project Program Grant (Principal Investigator), Linus Pauling Institute|
|2003-2013||NIH P01 AT002034 (Co-Project Leader, Project 1)|
Wei H, Zhang WJ, Leboeuf R, Frei B. (2014) Copper induces--and copper chelation by tetrathiomolybdate inhibits--endothelial activation in vitro. Redox Rep 19:40-48.
Wei H, Zhang WJ, McMillen TS, Leboeuf RC, Frei B. (2012) Copper chelation by tetrathiomolybdate inhibits vascular inflammation and atherosclerotic lesion development in apolipoprotein E-deficient mice. Atherosclerosis 223:306-313.
Zhang WJ, Wei H, Tien YT, Frei B. (2011) Genetic ablation of phagocytic NADPH oxidase in mice limits TNFalpha-induced inflammation in the lungs but not other tissues. Free Radic Biol Med 50:1517-1525.
Lotito SB, Zhang WJ, Yang CS, Crozier A, Frei B. (2011) Metabolic conversion of dietary flavonoids alters their anti-inflammatory and antioxidant properties. Free Radic Biol Med 51:454-463.
Wei H, Frei B, Beckman JS, Zhang WJ. (2011) Copper chelation by tetrathiomolybdate inhibits lipopolysaccharide-induced inflammatory responses in vivo. Am J Physiol Heart Circ Physiol 301:H712-720.
Zhang WJ, Wei H, Frei B (2010) The iron chelator, desferrioxamine, reduces inflammation and atherosclerotic lesion development in experimental mice. Exp Biol Med 235:633-641.
Zhang WJ, Wei H, Frei B (2009) Genetic deficiency of NADPH oxidase does not diminish, but rather enhances, LPS-induced acute inflammatory responses in vivo. Free Radic Biol Med 46:791-798.
Zhang WJ, Bird KE, McMillen TS, LeBoeuf RC, Hagen TM, Frei B (2008) Dietary alpha-lipoic acid supplementation inhibits atherosclerotic lesion development in apolipoprotein E-deficient and apolipoprotein E/low-density lipoprotein receptor-deficient mice. Circulation 117:421-428.
Zhang W, Wei H, Hagen T, Frei B (2007) Alpha-lipoic acid attenuates LPS-induced inflammatory responses by activating the phosphoinositide 3-kinase/Akt signaling pathway. Proc Natl Acad Sci USA 104:4077-4082.