A study led by UCL (University College London) scientists has designed a new drug that inhibits the adverse effects of C reactive protein (CRP), a protein that contributes to tissue damage in heart attacks and strokes. The findings, published in the journal Nature, suggest that targeting CRP may produce both immediate and long-term clinical benefits following a heart attack.
CRP is normally present at trace levels in the blood but its concentration increases sharply in almost all diseases including trauma, infection, strokes and chronic illnesses such as rheumatoid arthritis and Crohn’s disease. CRP levels also rise dramatically after a heart attack. Patients with the greatest and most persistent increases in CRP concentration suffer higher mortality, and CRP is always deposited in and around the damaged heart tissue.
Inflammation contributes significantly to the extent of heart attack damage and this can be exacerbated by CRP. The UCL team has previously shown that human CRP increases the severity of damage in experimental models of heart attack and stroke. This first identified CRP as a valid therapeutic target. The present collaborative study has now rationally designed a potent small molecule inhibitor of CRP.
Jenny Gimpel | alfa
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