6533b824fe1ef96bd128008b
RESEARCH PRODUCT
Molecular basis of endothelial dysfunction in sepsis.
Kirsten PetersJoachim BrunnerC. James KirkpatrickRonald E. Ungersubject
MaleEndotheliumPhysiologymedicine.medical_treatmentReceptors Cell SurfaceBiologyNitric OxidePathogenesisSepsisPhysiology (medical)SepsismedicineHumansEndothelial dysfunctionHypoxiaMembrane GlycoproteinsToll-Like ReceptorsEndothelial Cellsmedicine.diseaseReview articleBacterial adhesinEndotoxinsmedicine.anatomical_structureCytokineImmunologyMutationCytokinesFemaleDisease SusceptibilityEndothelium VascularCardiology and Cardiovascular MedicineReactive Oxygen SpeciesCell Adhesion MoleculesIntracellularInterleukin-1description
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.
| year | journal | country | edition | language |
|---|---|---|---|---|
| 2003-10-15 | Cardiovascular research |