The DOI matches its Crossref record; 14 of the 14 references it cites were found in a registry or an index.
Harmful molecular mechanisms in sepsis
Open accessAbstract
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.
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BackgroundA network-based analysis of systemic inflammation in humans
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The acute respiratory distress syndrome
Matthay, M. A., Ware, L. B., & Zimmerman, G. A. (2012) · Journal of Clinical Investigation · doi:10.1172/jci60331 · Cited by 1,706
Liver inflammation and fibrosis
Koyama, Y., & Brenner, D. A. (2017) · Journal of Clinical Investigation · doi:10.1172/jci88881 · Cited by 1,295
The immune system’s role in sepsis progression, resolution, and long-term outcome
Delano, M. J., & Ward, P. A. (2016) · Immunological Reviews · doi:10.1111/imr.12499 · Cited by 880
Self-citationMei, S. H. J., Haitsma, J. J., Dos Santos, C. C., Deng, Y., Lai, P. F. H., Slutsky, A. S., Liles, W. C., & Stewart, D. J. (2010) · American Journal of Respiratory and Critical Care Medicine · doi:10.1164/rccm.201001-0010oc · Cited by 721
Metadata
- Authors
- Rittirsch, D., Flierl, M. A., & Ward, P. A.
- Venue
- Nature Reviews Immunology
- Published
- 2008-10
- Volume
- 8
- Issue
- 10
- Pages
- 776-787
- ISSN
- 1474-1733 (ISSN-L)
- 1474-1741
- OpenAlex
- W1981243375
- Cited by
- 1,202
- References
- 14
- FWCI
- 7.97
- Type
- journal article
- Language
- en
- Open access
- green
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Bibliographic data: Semantic Scholar, OpenAlex, Crossref.
Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
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