Harmful molecular mechanisms in sepsis
By D. Rittirsch, M. Flierl, P. Ward. Nature reviews. Immunology, 2008
1,230 citations recorded by the source corpus.
Sepsis and sepsis-associated multi-organ failure are major challenges for scientists and clinicians and are a tremendous burden for health-care systems. Despite extensive basic research and clinical studies, the pathophysiology of sepsis is still poorly understood. We are now beginning to understand that sepsis is a heterogeneous, dynamic syndrome caused by imbalances in the 'inflammatory network'. In this Review, we highlight recent insights into the molecular interactions that occur during sepsis and attempt to unravel the nature of the dysregulated immune response during sepsis.
Subfields: Critical Care and Intensive Care Medicine, Epidemiology, Immunology
View Paper: https://www.semanticscholar.org/paper/737a55256205cef042ed588472bc1eea724d8c22
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Citations in the corpus
- Molecular Intercommunication between the Complement and Coagulation Systems (2010, background): “Furthermore, both systems belong to a complex inflammatory network (3) and exhibit some similar characteristics regarding the specialized functions of their activators and inhibitors.”
- Liver inflammation and fibrosis. (2017, background): “Immune cells are activated by endogenous danger signals known as alarmins (18) or damage-associated molecular patterns (DAMPs), which are released by dead or damaged cells (19, 20).”
- The Complement System (2010, background): “In sepsis, excessive C5a generation is thought to contribute to increased thymocyte apoptosis and consumptive coagulopathy, decreased innate immune functions of neutrophils, cardiomyopathy and multiple organ failure (for review, see Rittirsch et al. 2008b).”