Fibrin(ogen) and its fragments in the pathophysiology and treatment of myocardial infarction.
The occlusion of a coronary artery leads to ischemia of the myocardium, while permanent occlusion results in cell death and myocardial dysfunction. Early restoration of blood flow is the only means to reduce or prevent myocardial necrosis, but-paradoxically-reperfusion itself contributes to injury of the heart. In animal models, this phenomenon is well described, and there are many different unrelated approaches to reduce reperfusion injury. In humans, however, pharmacological interventions have so far failed to reduce myocardial reperfusion injury. We summarize the pathogenesis of reperfusion injury, detailing the role of fibrin(ogen) and its derivatives. Moreover, we introduce a new concept for fibrin derivatives as potential targets for reperfusion therapy.
Zacharowski
Kai
K
Molecular Cardioprotection and Inflammation Group, Department of Anesthesia, University Hospital of Düsseldorf, Moorenstrasse 5, 40225, Düsseldorf, Germany. kai.zacharowski@uni-duesseldorf.de
Zacharowski
Paula
P
Reingruber
Sonja
S
Petzelbauer
Peter
P
D000818:Animals; D000893:Anti-Inflammatory Agents / Q000627:therapeutic use; D005337:Fibrin / Q000378:metabolism*; D005338:Fibrin Fibrinogen Degradation Products / Q000378:metabolism; D005340:Fibrinogen / Q000378:metabolism*; D006801:Humans; D007249:Inflammation / Q000188:drug therapy / Q000378:metabolism; D009203:Myocardial Infarction / Q000209:etiology* / Q000473:pathology / Q000628:therapy*; D015428:Myocardial Reperfusion Injury / Q000209:etiology* / Q000473:pathology / Q000628:therapy*; D009206:Myocardium / Q000276:immunology / Q000473:pathology
D000893:Anti-Inflammatory Agents; D005338:Fibrin Fibrinogen Degradation Products; D005337:Fibrin; D005340:Fibrinogen