The potential of monoclonal antibodies to reduce reperfusion injury in myocardial infarction

Marcus E. McKenzie, Paul A. Gurbel

Research output: Contribution to journalReview articlepeer-review

Abstract

Reperfusion injury is mediated, in part, by the accumulation of platelets and leucocytes in the microvasculature after reflow. These components of the blood pool form aggregates that can obstruct flow in small vessels. In addition, mediators released from leucocytes and platelets further damage the reperfused myocardium. A strategy to limit reperfusion injury exploits the important role of membrane-bound adhesion molecules that attach platelets and leucocytes to themselves and to the vascular endothelium. Monoclonal antibodies against specific adhesion receptors effectively eliminate the function of the receptor. The most widely investigated receptors are P-selectin, present on platelets and the endothelium, CD11/CD18, present on leucocytes, and the fibrinogen receptor on platelets. Numerous animal studies have strongly supported the use of these monoclonal antibodies to block adhesion receptors as adjunctive reperfusion therapy. However, recent human trials have yielded disappointing results.

Original languageEnglish (US)
Pages (from-to)395-404
Number of pages10
JournalBioDrugs
Volume15
Issue number6
DOIs
StatePublished - 2001

ASJC Scopus subject areas

  • Biotechnology
  • Pharmacology
  • Pharmacology (medical)

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