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Zang, Mengwei
Zang lab members

Contact

210-562-4213

zang@uthscsa.edu

Programs

  • M.D./Ph.D. in South Texas Medical Scientist Training Program
  • M.S. in Personalized Molecular Medicine
  • Ph.D. in Integrated Biomedical Sciences
  • Biochemical Mechanisms in Medicine
  • Biology of Aging
  • Physiology and Pharmacology

Departments & Divisions

  • Department of Molecular Medicine

Institutes & Centers

  • Sam and Ann Barshop Institute for Longevity and Aging Studies

Currently seeking M.S. & Ph.D. students

Mengwei Zang, M.D., Ph.D.

Professor

The Ewing Halsell Distinguished Chair

Associate Director - MD/PhD Program, UT Health San Antonio

Dr. Mengwei Zang is a faculty member in the Sam and Ann Barshop Institute for Longevity and Aging as well as the Department of Molecular Medicine. The Zang lab focuses on the molecular mechanisms underlying obesity, diabetes and chronic liver disease related to aging.

Zang lab seeks to develop new therapeutic strategies for obesity, diabetes, and fatty liver disease by building a better understanding of molecular mechanisms of nutrient sensing network. Studies from Zang laboratory have identified several nutrient sensors, such as AMP-activated protein kinase (AMPK), the NAD-dependent deacetylase (SIRT1), mechanistic target of rapamycin (mTOR), and the hepatocyte-derived hormone FGF21. Dysregulation of AMPK or SIRT1 signaling appears to be involved in the pathogenesis of fatty liver disease and adipose tissue fibrosis in obesity and type 2 diabetes. Zang Lab has also elucidated AMPK-dependent inhibition of de novo lipogenesis as a molecular mechanism for the beneficial effects of metformin, the most widely prescribed type 2 diabetes drugs, and polyphenols, on hepatic steatosis, hyperlipidemia, and atherogenesis in type 1 and type 2 diabetes. Further studies demonstrated that SIRT1 is functionally linked to FGF21 and the regulation of fatty acid metabolism, providing major therapeutic targets for the treatment of fatty liver disease. These important findings were published in high impact journals such as Cell Metabolism, Gastroenterology, Hepatology, and Diabetes.

Zang Lab’s research utilizes a variety of biochemical, cellular biology, metabolic and screening approaches both in cell culture and whole animals to identify the molecular mechanisms by which mammalian cells sense, communicate, and respond to nutrients. The ultimate goal is to provide new insight into the pathological mechanisms of diabetes and obesity as well as to identify potential therapeutic interventions of metabolic disease and age-associated metabolic diseases.

 

Other profile: See more at: https://barshopinstitute.uthscsa.edu/team-member/zang-mengwei/

  • Professional Background

    Education

    • 2003 - Postdoctoral Fellowship - Diabetes and Signal Transduction - Boston University School of Medicine
    • 1999 - Postdoctoral Fellowship - Gastroenterology and Pharmacology - Mayo Clinic College of Medicine
    • 1998 - PhD - Pharmacology - Chinese Academy of Medical Sciences & Peking Union Medical College
    • 1987 - MS - Pathophysiology - Henan Medical University
    • 1984 - MD - Medicine - Wannan Medical College

    Appointments

    • 2004-2010 - Assitant Professor of Medicine - Boston University School of Medicine, Boston, MA.
    • 2011-2015 - Associate Professor of Medicine - Boston University School of Medicine, Boston, MA.
    • 2016-2019 - Associate Professor of Molecular Medicine - University of Texas Health Science Center San Antonio, San Antonio, TX
    • 2020-present - Professor of Molecular Medicine - University of Texas Health Science Center San Antonio, San Antonio, TX
  • Instruction & Training

    • 2016 - Present, Post-Doctoral Student Supervision, UT Health Science Center at San Antonio
    • 2016 - Present, Post-Doctoral Student Supervision, UT Health Science Center at San Antonio
    • 2016 - Present, Pre-Doctoral Student Supervision, UT Health Science Center at San Antonio
    • 2016 - Present, High School/Junior High School Student Supervision, UT Health Science Center at San Antonio
    • 2016 - Present, Biomedical Science (IBMS 5000), UT Health San Antonio
    • 2016 - Present, Ph.D. Dissertations Directed, UT Health Science Center at San Antonio
  • Research & Grants

    Grants

     

    Federal

     

    Funding Agency NIH/NIDDK

    Title: Hepatokine Control of Metabolic Crosstalk and Insulin Resistance

    The major goal of this project is to understand how the NAD+-dependent deacetylase SIRT1 regulates hepatokines that are secreted by the liver and whether this process affects the progression of non-alcoholic fatty liver disease and diabetes.

     

    Funding Agency NIH/NIAAA

    Title: Alcohol-induced Dysregulation of Thiol Homeostasis and Endothelial Function

    The major goal of this study is to investigate whether Glutaredoxin-1, a specific de-glutathionylation thioreductase, controls redox hemostasis and improves chronic alcohol-induced endothelial dysfunction.

     

    Funding Agency NIH/NIDDK

    Title: Retinoic Acid receptor, Lipid Metabolism, and Fatty Liver Disease

    The overall objective of this project is to define the metabolic consequence, intervention, and mechanism of vitamin A-related retinoic acid receptor on non-alcoholic fatty liver disease (NAFLD),one of the most common chronic liver diseases in the United States.

     

    Funding Agency American Diabetes Association

    Title: Retinoic Acid Receptor Functions as a Novel Regulator of Lipid Metabolism in Diabetes

    The major goal of this ADA Basic Science Award is to investigate the effect of retinoic acid receptor on whole-body energy balance and insulin resistance in diabetes and obesity, a major public health issue in more than one-third adults (over 72 million people) in the United States.

  • Service

    Institutional

     

    Associate Director of the MSTP (MD/PhD) Program

    University of Texas Health Science Center at San Antonio,

    San Antonio, TX

    National

     

    Regular Members for NIH Study Sections/Grant Review Committee Appointments       

    NIH/NIDDK Grant Review Committee, Diabetes, Endocrinology and Metabolic Disease (DDK-B) Study Section

    The Research Grant Review Committee (RGRC) for the American Diabetes Association (ADA)

    American Heart Association (AHA) Grant Committee, Molecular Signaling-Basic Science 3

     

    Global

     

    Editorial Boards

     

    FASEB Journal (Impact Factor, 5.595)

    Hepatology (Impact Factor, 14.95)

  • Publications

       

      Selective Publications

       

      Morita M, Siddiqui N, Katsumura S, Rouya C, Larsson O, Nagashima T, Hekmatnejad B, Takahashi A, Kiyonari H, Zang M, St-Arnaud R, Oike Y, Giguère V, Topisirovic I, Okada-Hatakeyama M, Yamamoto T, Sonenberg N. Hepatic posttranscriptional network comprised of CCR4–NOT deadenylase and FGF21 maintains systemic metabolic homeostasis. Proceedings of the National Academy of Sciences. 2019; 116: 7973-7981.PMID: 30926667.

      Hongdong Wang H, Shen L, Sun X, , Liu F, Feng W, Jiang C, Chu X, Ye X, Jiang C, Wang Y, Pengzi Zhang P, Zang M, Zhu D, Bi Y. Adipose group 1 innate lymphoid cells promote adipose tissue fibrosis and diabetes in obesity. Nature Communications. 2019; 10 (1):3254. doi: 10.1038/s41467-019-11270-1.

      Chen H, Shen F, Sherban A, Nocon A, Li Y, Wang H, Rui X, Han J, Jiang B, Li N, Keyhani-Nejad F, Fan J, Liu F, Kamat A, Musi N, Pacher P, Gao B, Zang M. DEP domain-containing mTOR-interacting protein suppresses lipogenesis and ameliorates hepatic steatosis and acute-on-chronic liver injury in alcoholic liver disease. Hepatology. 2018; 68:496-514.

      Ramirez T, Li YM, Yin S, Xu MJ, Feng D, Zhou Z, Zang M, Mukhopadhyay P, Varga ZV, Pacher P, Gao B, Wang H. Aging aggravates alcoholic liver injury and fibrosis in mice by downregulating Sirtuin 1 expression. J Hepatol. 2017; 66: 601-609. 

      Luo T, Nocon A, Fry J, Sherban A, Rui X, Jiang B, Xu XJ, Han J, Yan Y, Yang Q, Li Q, Zang M. AMPK activation by metformin suppresses abnormal adipose tissue extracellular matrix remodeling and ameliorates insulin resistance in obesity. Diabetes. 2016; 65:2295-2310. 

      Han J, Weisbrod RM, Shao D, Watanabe Y, Yin X, Bachschmid MM, Seta F, Janssen-Heininger YM, Matsui R, Zang M, Hamburg NM, Cohen RA. The redox mechanism for vascular barrier dysfunction associated with metabolic disorders: Glutathionylation of Rac1 in endothelial cells. Redox Biology. 2016; 306-319. doi: 10.1016/j.redox.2016.09.003. 

      Gong Q, Hu Z, Zhang F, Cui A, Chen X, Jiang H, Gao J, Chen X, Han Y, Liang Q, Ye D, Shi L, Eugene Chin Y, Wang Y, Xiao H, Guo F, Liu Y, Zang M, Xu A, Li Y. Fibroblast Growth Factor 21 Improves Hepatic Insulin Sensitivity by Inhibiting Mammalian Target of Rapamycin Complex 1. Hepatology. 2016; 64:425-438.

      Li XY, Kover K, Heruth D, Watkins DJ, Moore WV, Zang M, Clements M, and Yun Yan. New insight into metformin action: regulation of ChREBP and FoXO1 activities in endothelial cells. Molecular Endocrinology. 2015; 29:1184-94.

      Li Y, Wong K, Giles A, Lee JW, Jiang J, Adams AC, Kharitonenkov A, Yang Q, Gao B, Guarente L, Zang M. Hepatic SIRT1 attenuates hepatic steatosis and controls energy balance in mice by inducing fibroblast growth factor 21. Gastroenterology. 2014; 146: 539-549.

      Li Y, Xu S, Jiang B, Cohen RA, Zang M* (*Corresponding author). Activation of sterol regulatory element binding protein and NLRP3 inflammasome in atherosclerotic lesion development in diabetic pigs. PLoS One. 2013; 8: e67532. doi:10.1371. PMID: 23825667.

      Li Y, Wong K, Walsh K, Gao B, Zang M. Retinoic acid receptor β stimulates hepatic induction of fibroblast growth factor 21 to promote fatty acid oxidation and control whole-body energy homeostasis in mice. Journal of Biological Chemistry. 2013; 288: 10490-10540.

      Li Y,  Xu S, Mihaylova M, Zheng B, Hou X, Jiang B, Park O, Luo Z, Lefai E, Shyy JY, Gao B, Wierzbicki M, Verbeuren TJ, Shaw RJ, Cohen RA, Zang M. AMPK phosphorylates and inhibits SREBP activity to attenuate hepatic steatosis and atherosclerosis in diet-induced insulin resistant mice. Cell Metabolism. 2011; 13: 376-388. Selected as the most cited article in Cell Metabolism in 2011

      Li Y, Xu S, Giles A, Nakamura K, Lee JW, Hou X, Donmez G, Li J, Luo Z, Walsh K, Guarente L, Zang M. Hepatic overexpression of SIRT1 in mice attenuates endoplasmic reticulum stress and insulin resistance in the liver. FASEB Journal. 2011; 25: 1664-1679.

      Hou X, Xu S, Maitland-Toolan KA, Sato K, Jiang B, Ido Y, Lan F, Walsh K, Wierzbicki M, Verbeuren TJ, Cohen RA, Zang M. SIRT1 regulates hepatocyte lipid metabolism through activating AMP-Activated protein kinase. Journal of Biological Chemistry. 2008; 283: 20015-20026. Faculty of 1000 Biology.

       

      Book Chapter

       

      Zang M. Chapter 2: The molecular basis of hepatic de novo lipogenesis in insulin resistance. In: James
      M. Ntambi PhD, eds. Hepatic De novo Lipogenesis and Regulation of
      Metabolism. 2015.

       

      Editorial

       

      Zang M. Targeting AMPK-SREBP nutrient sensing pathway has the therapeutic
      implication on insulin resistance and metabolic syndrome Chinese Journal
      of Diabase Mellitus 2015 Jan;7:200-204.

       

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