Versiti - Roy L. Silverstein, MD | Versiti Blood Research Institute

Roy L. Silverstein, MD

Roy L.  Roy L.  profile

Roy L. Silverstein, MD

Senior Investigator

Transfusion Medicine, Vascular Biology & Cell Therapy

Professor and Chairman Emeritus
Department of Medicine
Medical College of Wisconsin

Education and training

MD, Emory University School of Medicine, 1979
Residency in Internal Medicine, Hematology and Medical Oncology, New York Hospital Cornell Medical Center

Contact Information
  • 414-955-0518
  • 414-955-0518
  • Platelet and macrophage biology and atherothrombosis, with emphasis on molecular mechanisms through which the innate immune receptor CD36 mediates pro-thrombotic and pro-atherogenic signaling events in platelets and macrophages in the setting of chronic inflammation.  Recent focus has been on mitochondrial metabolic reprogramming and redox stress.

    Ongoing Research Support
    • 1R01HL164460-01A1  Silverstein/Chen/Shapiro (MPI) 04/01/23-03/31/27. NKA/CD36 signaling in adipocytes promotes oxidative stress and drives chronic inflammation in atherosclerosis.
      Role: Communicating PI
    • 1R01HL153397-01A1 Silverstein/Cui (MPI) 04/01/2021-03/31/2025. Pim1 kinase coordinates PPAR gamma pathway and mitochondrial function to mediate pro- atherogenic responses in macrophages.
      Role: Communicating PI

    Mirza Ahmar Beg, PhD
    Postdoctorall Fellow

    Yiqiong Zhao
    Research Lab Technician

    Complete list of Published Work (217 papers in MyBibliography: H index = 72 (~20,000 citations)

    MyNCBI (Click Here)

    Selected Publications
    1. Febbraio M, Podrez EA, Smith JD, Hazen SL, Hoff HF, Sharma K, Hajjar DP, and Silverstein RL. Targeted disruption of the Class B scavenger receptor, CD36, protects against atherosclerotic lesion development in mice. J. Clin. Invest. 2000. 105:1049-1056. PMCID: PMC300837.
    2. Jimenez B, Volpert OV, Crawford SE, Febbraio M, Silverstein RL and NP Bouck. Signals leading to apoptosis-dependent inhibition of neovascularization by thrombospondin-1. Nature Medicine 2000; 6:41-48.
    3. Rahaman SO, Lennon DJ, Febbraio M, Podrez EA, Hazen SL, Silverstein RL. CD36-dependent activation of c-Jun N-terminal kinase by oxidized LDL is required for macrophage foam cell formation. Cell Metabolism 2006;4(3):211-221. PMCID: PMC1855263.
    4. Park YM, Febbraio M, Silverstein RL. CD36 modulates macrophage migration in response to oxidized LDL: A mechanism of macrophage trapping. J. Clin. Invest. 2009; 119(1):136-145. PMCID: PMC2613464.
    5. Podrez EA, Byzova TV, Febbraio M, Salomon RG, Ma Y, Valiyaveettil M, Poliakov E, Sun M, Finton PJ, Curtis BR, Chen J, Zhang R, Silverstein RL, and SL Hazen. Platelet CD36 links hyperlipidemia, oxidant stress and a pro-thrombotic phenotype. Nature Medicine 2007; 13(9):1086-1095. PMCID: PMC3042888.
    6. Ghosh A, Li W, Febbraio M, Espinola RG, Cotrell E, McCrae K, and Silverstein RL. Platelet CD36 mediates interactions with endothelial cell-derived microparticles and contributes to thrombosis in vivo. J. Clin. Inv. 2008;118(5):1934-1943. PMCID: PMC2323190.
    7. Ren B, Hale J, Srikanthan S, Silverstein RL. Lysophosphatidic Acid Suppresses Endothelial Cell CD36 Expression and Promotes Angiogenesis via a PKD-1 Dependent Signaling Pathway. Blood 2011;117(22):6036-45. PMCID: PMC3112047
    8. Yang M, Cooley BC, Li W, Chen Y, Vasquez-Vivar J, Scoggins NO, Cameron S, Morrell CN, Silverstein RL. Platelet CD36 Promotes Thrombosis by Activating Redox Sensor ERK5 in Hyperlipidemic Conditions. Blood. 2017 May 25; 129(21):2917-2927. PMCID: PMC5445574.
    9. Chen Y, Huang W, Yang M, Xin G, Cui W, Xie Z, Silverstein RL. Cardiotonic Steroids Stimulate Macrophage Inflammatory Responses Through a Pathway Involving CD36, TLR4, and Na/K-ATPase. Arterioscler Thromb Vasc Biol. 2017; 37(8):1462-1469. PMCID: PMC5532064.
    10. Chen Y, Yang M, Huang W, Chen W, Zhao Y, Schulte ML, Volberding P, Gerbec Z, Zimmermann MT, Zeighami A, Demos W, Zhang J, Knaack D, Smith BC, Cui W, Malarkannan S, Sodhi K, Shapiro JI, Xie J, Sahoo D, Silverstein RL. Mitochondrial metabolic reprogramming by CD36 signaling drives macrophage inflammatory responses. Circ Res. 2019 Dec 6, 125:1087-1102. PMCID: PMC6921463.
    11. Dai W, Zhang H, Lund H, Zhang S, Castleberry M, Rodriguez M, Kuriakose G, Gupta S, Lewandowska M, Powers HR, Valmiki S, Zhu J, Shapiro AD, Hussain MM, López JA, Sorci-Thomas MG, Silverstein RL, Ginsberg HN, Sahoo D, Tabas I, Zheng Z. Intracellular tPA-PAI-1 interaction determines VLDL assembly in hepatocytes.  Science 2023; Sep;381(6661):eadh5207.
    Thrombosis & Hemostasis
    We study the properties of blood that cause it to clot. Our findings help to treat diseases that cause blood clots or excessive bleeding.
    Join Versiti Blood Research Institute
    Versiti Blood Research Institute, located in Milwaukee, Wisconsin, includes basic and clinical researchers in a variety of blood health fields.
    Our Investigators
    Browse our Investigators, Emeritus Investigators, and other members of the Blood Research Institute.
    Versiti Blood Research Institute
    Versiti Blood Research Institute investigators study blood disorders like hemophilia, blood cancers like leukemia, and other blood diseases.