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Targeting C-reactive protein for the treatment of cardiovascular disease

Author

Listed:
  • Mark B. Pepys

    (Royal Free and University College Medical School, University College London)

  • Gideon M. Hirschfield

    (Royal Free and University College Medical School, University College London
    Addenbrookes Hospital)

  • Glenys A. Tennent

    (Royal Free and University College Medical School, University College London)

  • J. Ruth Gallimore

    (Royal Free and University College Medical School, University College London)

  • Melvyn C. Kahan

    (Royal Free and University College Medical School, University College London)

  • Vittorio Bellotti

    (Royal Free and University College Medical School, University College London
    Universitá di Pavia)

  • Philip N. Hawkins

    (Royal Free and University College Medical School, University College London)

  • Rebecca M. Myers

    (University of Cambridge)

  • Martin D. Smith

    (University of Cambridge)

  • Alessandra Polara

    (University of Cambridge)

  • Alexander J. A. Cobb

    (Royal Free and University College Medical School, University College London
    University of Reading)

  • Steven V. Ley

    (University of Cambridge)

  • J. Andrew Aquilina

    (University of Cambridge
    University of Wollongong)

  • Carol V. Robinson

    (University of Cambridge)

  • Isam Sharif

    (University of Edinburgh)

  • Gillian A. Gray

    (University of Edinburgh)

  • Caroline A. Sabin

    (Royal Free and University College Medical School, University College London)

  • Michelle C. Jenvey

    (University of Southampton)

  • Simon E. Kolstoe

    (University of Southampton)

  • Darren Thompson

    (University of Southampton
    University of Sussex)

  • Stephen P. Wood

    (University of Southampton)

Abstract

Aiming for the heart C-reactive protein (CRP) is a clinical marker for inflammatory disease and infection, but it also binds to damaged cells and activates complement, a host defence and pro-inflammatory system of serum proteins. Complement-mediated inflammation exacerbates tissue injury in heart attacks, and human CRP increases damage in a rat model of acute myocardial infarction via a complement-dependent mechanism. These observations point to CRP as a possible target for drugs intended to protect the heart. Pepys et al. therefore designed a specific small-molecule CRP inhibitor. Five molecules of this palindromic compound are bound by two pentameric CRP molecules arranged face-to-face, as in the X-ray crystal structure of the complex on the cover. The inhibitor blocks the adverse effects of human CRP in rats with acute myocardial infarction, suggesting that early therapeutic inhibition of CRP might be beneficial for heart attack patients.

Suggested Citation

  • Mark B. Pepys & Gideon M. Hirschfield & Glenys A. Tennent & J. Ruth Gallimore & Melvyn C. Kahan & Vittorio Bellotti & Philip N. Hawkins & Rebecca M. Myers & Martin D. Smith & Alessandra Polara & Alexa, 2006. "Targeting C-reactive protein for the treatment of cardiovascular disease," Nature, Nature, vol. 440(7088), pages 1217-1221, April.
    • Handle: RePEc:nat:nature:v:440:y:2006:i:7088:d:10.1038_nature04672
    DOI: 10.1038/nature04672
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    Cited by:

    1. Debbie A Lawlor & Roger M Harbord & Nic J Timpson & Gordon D O Lowe & Ann Rumley & Tom R Gaunt & Ian Baker & John W G Yarnell & Mika Kivimäki & Meena Kumari & Paul E Norman & Konrad Jamrozik & Graeme , 2008. "The Association of C-Reactive Protein and CRP Genotype with Coronary Heart Disease: Findings from Five Studies with 4,610 Cases amongst 18,637 Participants," PLOS ONE, Public Library of Science, vol. 3(8), pages 1-14, August.
    2. Carlos A Labarrere & John R Woods & James W Hardin & Beate R Jaeger & Marian Zembala & Mario C Deng & Ghassan S Kassab, 2014. "Early Inflammatory Markers Are Independent Predictors of Cardiac Allograft Vasculopathy in Heart-Transplant Recipients," PLOS ONE, Public Library of Science, vol. 9(12), pages 1-18, December.

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