The DOI matches its Crossref record; 9 of the 9 references it cites were found in a registry or an index.
Apoptosis in sepsis: a new target for therapeutic exploration
Abstract
The treatment of sepsis and septic shock remains a clinical conundrum, and recent prospective trials with biological response modifiers aimed at the inflammatory response have shown only modest clinical benefit. Recently, interest has shifted toward therapies aimed at reversing the accompanying periods of immune suppression. Studies in experimental animals and critically ill patients have demonstrated that increased apoptosis of lymphoid organs and some parenchymal tissues contributes to this immune suppression, anergy, and organ system dysfunction. During sepsis syndromes, lymphocyte apoptosis can be triggered by the absence of IL-2 or by the release of glucocorticoids, granzymes, or the so-called 'death' cytokines: tumor necrosis factor alpha or Fas ligand. Apoptosis proceeds via auto-activation of cytosolic and/or mitochondrial caspases, which can be influenced by the pro- and anti-apoptotic members of the Bcl-2 family. In experimental animals, not only can treatment with inhibitors of apoptosis prevent lymphoid cell apoptosis; it may also improve outcome. Although clinical trials with anti-apoptotic agents remain distant due in large part to technical difficulties associated with their administration and tissue targeting, inhibition of lymphocyte apoptosis represents an attractive therapeutic target for the septic patient.
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Cites
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Cited by
Gruver, A., Hudson, L., & Sempowski, G. (2007) · The Journal of Pathology · doi:10.1002/path.2104 · Cited by 834
Novel strategies for the treatment of sepsis
Riedemann, N. C., Guo, R.-F., & Ward, P. A. (2003) · Nature Medicine · doi:10.1038/nm0503-517 · Cited by 773
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Self-citationThe Neuropathology of Septic Shock
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Metadata
- Authors
- OBERHOLZER, C., OBERHOLZER, A., CLARE-SALZLER, M., & MOLDAWER, L. L.
- Venue
- The FASEB Journal
- Publisher
- Wiley
- Published
- 2001-04
- Volume
- 15
- Issue
- 6
- Pages
- 879-892
- ISSN
- 0892-6638 (ISSN-L)
- 1530-6860
- OpenAlex
- W2165509188
- Cited by
- 271
- References
- 9
- FWCI
- 16.40
- Type
- journal article
- Language
- en
- Open access
- closed
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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
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