The DOI matches its Crossref record; 15 of the 15 references it cites were found in a registry or an index.
Pyroptosis: host cell death and inflammation
Open accessAbstract
Eukaryotic cells can initiate several distinct programmes of self-destruction, and the nature of the cell death process (non-inflammatory or proinflammatory) instructs responses of neighbouring cells, which in turn dictates important systemic physiological outcomes. Pyroptosis, or caspase 1-dependent cell death, is inherently inflammatory, is triggered by various pathological stimuli, such as stroke, heart attack or cancer, and is crucial for controlling microbial infections. Pathogens have evolved mechanisms to inhibit pyroptosis, enhancing their ability to persist and cause disease. Ultimately, there is a competition between host and pathogen to regulate pyroptosis, and the outcome dictates life or death of the host.
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Cites
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Copper induces cell death by targeting lipoylated TCA cycle proteins
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Caspase-11 cleaves gasdermin D for non-canonical inflammasome signalling
Kayagaki, N., Stowe, I. B., Lee, B. L., O’Rourke, K., Anderson, K., Warming, S., Cuellar, T., Haley, B., Roose-Girma, M., Phung, Q. T., et al. (2015) · Nature · doi:10.1038/nature15541 · Cited by 3,686
Metadata
- Authors
- Bergsbaken, T., Fink, S. L., & Cookson, B. T.
- Venue
- Nature Reviews Microbiology
- Published
- 2009-02
- Volume
- 7
- Issue
- 2
- Pages
- 99-109
- ISSN
- 1740-1526 (ISSN-L)
- 1740-1534
- OpenAlex
- W1985970823
- Cited by
- 3,183
- References
- 15
- FWCI
- 3.81
- Type
- journal article
- Language
- en
- Open access
- green
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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
Semantic Scholar’s data is described in: Kinney, R., et al. (2023). The Semantic Scholar Open Data Platform. arXiv:2301.10140.
