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Targeting C-Reactive Protein For The Treatment Of Cardiovascular Disease, 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, Alexander J. A Cobb, Steven V. Ley, J. Andrew Aquilina, Carol V. Robinson, Isam Sharif, Gillian A. Gray, Caroline A. Sabin, Michelle C. Jenvey, Simon E. Kolstoe, Darren Thompson, Stephen P. Wood

J. A. Aquilina

Complement-mediated inflammation exacerbates the tissue injury of ischaemic necrosis in heart attacks and strokes, the most common causes of death in developed countries. Large infarct size increases immediate morbidity and mortality and, in survivors of the acute event, larger non-functional scars adversely affect long-term prognosis. There is thus an important unmet medical need for new cardioprotective and neuroprotective treatments. We have previously shown that human C-reactive protein (CRP), the classical acute-phase protein that binds to ligands exposed in damaged tissue and then activates complement1, increases myocardial and cerebral infarct size in rats subjected to coronary or cerebral artery ligation, respectively2,3. …