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Tang J, Lobatto ME, Hassing L, et al. Inhibiting macrophage proliferation suppresses atherosclerotic plaque inflammation. Sci Adv. 2015;1(3)doi: 10.1126/sciadv.1400223.
Tang, J., Lobatto, M. E., Hassing, L., van der Staay, S., van Rijs, S. M., Calcagno, C., Braza, M. S., Baxter, S., Fay, F., Sanchez-Gaytan, B. L., Duivenvoorden, R., Sager, H., Astudillo, Y. M., Leong, W., Ramachandran, S., Storm, G., Pérez-Medina, C., Reiner, T., Cormode, D. P., Strijkers, G. J., Stroes, E. S., Swirski, F. K., Nahrendorf, M., Fisher, E. A., Fayad, Z. A., & Mulder, W. J. (2015). Inhibiting macrophage proliferation suppresses atherosclerotic plaque inflammation. Science advances, 1(3), . https://doi.org/10.1126/sciadv.1400223
Tang, Jun, et al. "Inhibiting macrophage proliferation suppresses atherosclerotic plaque inflammation." Science advances vol. 1,3 (2015). doi: https://doi.org/10.1126/sciadv.1400223
Tang J, Lobatto ME, Hassing L, van der Staay S, van Rijs SM, Calcagno C, Braza MS, Baxter S, Fay F, Sanchez-Gaytan BL, Duivenvoorden R, Sager H, Astudillo YM, Leong W, Ramachandran S, Storm G, Pérez-Medina C, Reiner T, Cormode DP, Strijkers GJ, Stroes ES, Swirski FK, Nahrendorf M, Fisher EA, Fayad ZA, Mulder WJ. Inhibiting macrophage proliferation suppresses atherosclerotic plaque inflammation. Sci Adv. 2015 Apr;1(3). doi: 10.1126/sciadv.1400223. PMID: 26295063; PMCID: PMC4539616.
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Sci Adv. 2015 Apr;1(3). doi: 10.1126/sciadv.1400223.

Inhibiting macrophage proliferation suppresses atherosclerotic plaque inflammation.

Science advances

Jun Tang, Mark E Lobatto, Laurien Hassing, Susanne van der Staay, Sarian M van Rijs, Claudia Calcagno, Mounia S Braza, Samantha Baxter, Francois Fay, Brenda L Sanchez-Gaytan, Raphaël Duivenvoorden, Hendrik Sager, Yaritzy M Astudillo, Wei Leong, Sarayu Ramachandran, Gert Storm, Carlos Pérez-Medina, Thomas Reiner, David P Cormode, Gustav J Strijkers, Erik S G Stroes, Filip K Swirski, Matthias Nahrendorf, Edward A Fisher, Zahi A Fayad, Willem J M Mulder

Affiliations

  1. Translational and Molecular Imaging Institute, Icahn School of Medicine at Mount Sinai, New York 10029, NY, USA ; Graduate School of Biomedical Sciences, Icahn School of Medicine at Mount Sinai, New York, NY, USA.
  2. Translational and Molecular Imaging Institute, Icahn School of Medicine at Mount Sinai, New York 10029, NY, USA ; Department of Vascular Medicine, Academic Medical Center, Amsterdam 1105 AZ, The Netherlands.
  3. Translational and Molecular Imaging Institute, Icahn School of Medicine at Mount Sinai, New York 10029, NY, USA.
  4. Department of Vascular Medicine, Academic Medical Center, Amsterdam 1105 AZ, The Netherlands.
  5. Center for Systems Biology, Massachusetts General Hospital, and Division of Cardiovascular Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, MA 02114, USA.
  6. Department of Medicine (Cardiology) and Cell Biology, Marc and Ruti Bell Program in Vascular Biology, NYU School of Medicine, New York, NY 10016, USA.
  7. Department of Pharmaceutics, Utrecht Institute of Pharmaceutical Sciences, Utrecht University, Universiteitsweg 99, 3584 CG Utrecht, The Netherlands ; Department of Controlled Drug Delivery, MIRA Institute for Biomedical Engineering and Technical Medicine, University of Twente, 7500 AE Enschede, The Netherlands.
  8. Department of Radiology, Memorial Sloan-Kettering Cancer Center, 1275 York Ave., New York, NY 10065.
  9. Department of Radiology, University of Pennsylvania, Philadelphia, PA 19104, USA.
  10. Department of Biomedical Engineering and Physics, Academic Medical Center, Amsterdam, The Netherlands.

PMID: 26295063 PMCID: PMC4539616 DOI: 10.1126/sciadv.1400223

Abstract

Inflammation drives atherosclerotic plaque progression and rupture, and is a compelling therapeutic target. Consequently, attenuating inflammation by reducing local macrophage accumulation is an appealing approach. This can potentially be accomplished by either blocking blood monocyte recruitment to the plaque or increasing macrophage apoptosis and emigration. Because macrophage proliferation was recently shown to dominate macrophage accumulation in advanced plaques, locally inhibiting macrophage proliferation may reduce plaque inflammation and produce long-term therapeutic benefits. To test this hypothesis, we used nanoparticle-based delivery of simvastatin to inhibit plaque macrophage proliferation in apolipoprotein E deficient mice (

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