Endogenous and Natural Complement Inhibitor Attenuates Myocardial Injury and Arterial Thrombogenesis

Coagulation disorders and reperfusion of ischemic myocardium are major causes of morbidity and mortality. Lectin pathway initiation complexes are composed of multimolecular carbohydrate recognition subcomponents and 3 lectin pathway–specific serine proteases. We have recently shown that the lectin pathway–specific carbohydrate recognition subcomponent mannose-binding lectin plays an essential role in the pathophysiology of thrombosis and ischemiareperfusion injury. Thus, we hypothesized that the endogenous mannose-binding lectin (MBL)ficolin-associated protein-1 (MAP-1) that inhibits complement activation in vitro also could be an in vivo regulator by attenuating myocardial schemareperfusion injury and thrombogenesis when used at pharmacological doses in wild-type mice.