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Cardiovascular Research 2003 60(1):49-57; doi:10.1016/S0008-6363(03)00397-3
© 2003 by European Society of Cardiology
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Copyright © 2003, European Society of Cardiology

Molecular basis of endothelial dysfunction in sepsis

Kirsten Peters, Ronald E. Unger, Joachim Brunner and C.James Kirkpatrick*

Institute of Pathology, Johannes Gutenberg University of Mainz, Langenbeckstr. 1, 55101 Mainz, Germany

*Corresponding author. Tel.: +49-6131-17-7301; fax: +49-6131-17-6695. Email address: kirkpatrick{at}pathologie.klinik.uni-mainz.de

Sepsis is one of the major causes of mortality in critically ill patients and develops as a result of the host response to infection. A complex network of events is set into motion in the body by the infection and results in the pathogenesis of sepsis. This review article focuses on the molecular mechanisms and components involved in the pathogenesis of sepsis with a major emphasis on the endothelium. This includes sepsis-inducing bacterial components (e.g. endotoxins), cellular targets of these molecules and their responses, host reactions, intracellular and cytokine networks, individual susceptibility and new therapeutic targets in sepsis treatment.

KEYWORDS Sepsis; Infection/inflammation; Endothelial function; Cytokines; Endotoxins

Time for primary review 30 days.


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