Pyroptosis-Induced Inflammation and Tissue Damage
Open accessAbstract
Pyroptosis is a programmed necrotic cell death executed by gasdermins, a family of pore-forming proteins. The cleavage of gasdermins by specific proteases enables their pore-forming activity. The activation of the prototype member of the gasdermin family, gasdermin D (GSDMD), is linked to innate immune monitoring by inflammasomes. Additional gasdermins such as GSDMA, GSDMB, GSDMC, and GSDME are activated by inflammasome-independent mechanisms. Pyroptosis is emerging as a key host defense strategy against pathogens. However, excessive pyroptosis causes cytokine storm and detrimental inflammation leading to tissue damage and organ dysfunction. Consequently, dysregulated pyroptotic responses contribute to the pathogenesis of various diseases, including sepsis, atherosclerosis, acute respiratory distress syndrome, and neurodegenerative disorders. This review will discuss the inflammatory consequences of pyroptosis and the mechanisms of pyroptosis-induced tissue damage and disease pathogenesis.
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Pyroptosis is an inflammatory form of RCD mediated by activation of the inflammasome and caspase-1, resulting in gasdermin-mediated membrane pore formation and cytokine release.
“In contrast, pyroptosis is an inflammatory form of RCD mediated by activation of the inflammasome and caspase-1, resulting in membrane pore formation mediated by gasdermin and cytokine release [37,38].”
From Role of Regulated Cell Death Pathways in Snakebite Envenomation: Mechanisms, Crosstalk, and Therapeutic Opportunities (2026) · cites this paper as [38]
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Alangode, A., Rajasekhar, A., Sabu, J. J., Krishna, S., Anuja, D., Sreeja, A., Remesh, G., Kaladevi, A., & Nair, B. G. (2026) · International Journal of Molecular Sciences · doi:10.3390/ijms27156830
- Authors
- Vasudevan, S. O., Behl, B., & Rathinam, V. A.
- Affiliations
- UConn Health (US)
- Corresponding author
- Rathinam, Vijay A.
- Venue
- Seminars in Immunology
- Publisher
- Elsevier BV
- Published
- 2023-09
- Volume
- 69
- Pages
- 101781
- ISSN
- 1044-5323 (ISSN-L)
- PMC
- PMC10598759
- OpenAlex
- W4381548955
- Cited by
- 412
- References
- 9
- Citations by year
- 2026: 170 · 2025: 180 · 2024: 59 · 2023: 3
- FWCI
- 10.88
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- www.elsevier.com/tdm/userlicense/1.0/ (tdm)
- www.elsevier.com/legal/tdmrep-license (tdm)
- www.elsevier.com/open-access/userlicense/1.0/ (am, 294 d)
- doi.org/10.15223/policy-017 (stm-asf)
- doi.org/10.15223/policy-037 (stm-asf)
- doi.org/10.15223/policy-012 (stm-asf)
- doi.org/10.15223/policy-029 (stm-asf)
- doi.org/10.15223/policy-004 (stm-asf)
- Locations
- Seminars in Immunology (acceptedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institutes of Health (R01AI119015, R01AI148491)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Inflammasome and immune disorders
- Life Sciences › Immunology and Microbiology › Immunology › Immune Response and Inflammation
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Cell death mechanisms and regulation
- Keywords
- pyroptosis, gasdermin, gasdermin D, gasdermin E, GSDMB, GSDMA, inflammasome, cytokine storm, inflammation, tissue damage, sepsis, atherosclerosis, acute respiratory distress syndrome, neurodegenerative diseases, host defense against infection
- MeSH terms
- Pyroptosis, Gasdermins, Humans, Inflammation, Neoplasm Proteins, Biomarkers, Tumor, Apoptosis, Pore Forming Cytotoxic Proteins, Inflammasomes
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