Definition and research guide
This page combines a MeSH definition, publication statistics and selected research abstracts. It is a starting point for reading the literature, not a medical textbook or a systematic evidence review.
Content available: 3 complete abstracts (585 words), 9 references. Full article text is not stored or reproduced here; follow the PMID, DOI or PMC links to read the original sources and their access terms.
Definition
Type of programmed cell death associated with infection by intracellular pathogens. It is characterized by inflammasome formation; activation of caspase 1; and cytokines mediated inflammation.
Definition: NLM Medical Subject Headings (MeSH) scope note (Public domain (U.S. National Library of Medicine); attribution requested). View the MeSH record.
Also known as: Pyroptoses; Inflammatory Apoptosis; Apoptoses, Inflammatory; Apoptosis, Inflammatory; Inflammatory Apoptoses; Pyroptotic Cell Death; Cell Death, Pyroptotic; Cell Deaths, Pyroptotic.
Where it fits in the MeSH classification
- Broader topics
- Apoptosis
- See also
- Necrosis
Related concepts
- Inflammasome
- Caspase
- Cytokines
Research landscape
PubMed indexes 8,439 records tagged with the MeSH heading “Pyroptosis” (counts retrieved 2026-10-29). 7,815 of them (92.6%) were published from 2020 onward, and the busiest period so far is 2020 onward with 7,815 records.
Reviews account for 1,280 records (15.2%) and meta-analyses for 0. Randomized controlled trials number 10 (0.1%) as a share of all records on the topic. Randomized trials make up only a small share of this literature, so much of what is known comes from laboratory, observational or descriptive work.
Show the data
| Period | Records |
|---|---|
| through 1999 | 0 |
| 2000-2009 | 0 |
| 2010-2019 | 674 |
| 2020 onward | 7,815 |
Publication-type chart data
| Type | Records | Share |
|---|---|---|
| Reviews | 1,280 | 15.2% |
| Meta-analyses | 0 | 0.0% |
| Randomized controlled trials | 10 | 0.1% |
Method: PubMed query "Pyroptosis"[MeSH Terms] with publication-type and date filters, retrieved 2026-10-29.
Reading the evidence in molecular biology
Molecular biology establishes mechanisms through controlled experiments, often in simplified systems such as purified proteins, cultured cells or model organisms. Such work can show what is possible in a defined system, but whether a pathway matters in a whole organism or in human disease needs further evidence. Check the experimental system, whether findings were reproduced by independent groups, and whether the authors tested the mechanism directly or inferred it from correlation.
Evidence from open-access studies
These open-access studies come from PubMed’s best-match results for this heading (papers whose main topic it is), ranked here by citation count, with one recent addition. Each abstract is reproduced in full under its recorded open licence so that you can read the authors’ own words. They illustrate the literature; they are not a systematic summary of it. Citation counts measure attention, not reliability or clinical benefit.
| Study / authors | Year | Source label / design | Europe PMC citations | Licence / source |
|---|---|---|---|---|
| Pyroptosis-driven immune dysregulation in COPD: molecular mechanisms and therapeutic implications | 2025 | Review article Design not recorded in structured metadata | 11 | cc by PMID 41476973 · DOI · PMC12747962 |
| H3K18 lactylation-mediated SPHK1-SIRT1 feedback loop accelerates pyroptosis of tubular epithelial cells in sepsis-associated acute kidney injury | 2026 | Research article Design not recorded in structured metadata | 10 | cc by PMID 41799201 · DOI · PMC12964219 |
| Pyroptosis-immune cell cross talk in asthma: From molecular mechanisms to precision therapeutics | 2025 | Review article Design not recorded in structured metadata | 8 | cc by PMID 41394843 · DOI · PMC12698424 |
Pyroptosis-driven immune dysregulation in COPD: molecular mechanisms and therapeutic implications [1]
Abstract reading summary — source excerpts
- Opening excerpt
- Pyroptosis, a programmed cell death mechanism mediated by gasdermin proteins such as GSDMD, is typically activated by inflammasomes.
- Closing excerpt
- By synthesizing evidence from primary research, we highlight how pyroptosis influences immune dysregulation in COPD and propose novel strategies for disease management.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (101 words)
Pyroptosis, a programmed cell death mechanism mediated by gasdermin proteins such as GSDMD, is typically activated by inflammasomes. While essential for host defense against infections, excessive pyroptosis contributes to chronic inflammation and exacerbates inflammatory diseases. In chronic obstructive pulmonary disease (COPD), dysregulated pyroptosis interacts with immune cells-including neutrophils, macrophages, and T lymphocytes-to perpetuate inflammation, tissue damage, and acute exacerbations. This review explores the molecular mechanisms of pyroptosis, its cell-type-specific roles in COPD pathogenesis, and its implications for therapeutic targeting. By synthesizing evidence from primary research, we highlight how pyroptosis influences immune dysregulation in COPD and propose novel strategies for disease management.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 41476973 · DOI · PMC12747962
H3K18 lactylation-mediated SPHK1-SIRT1 feedback loop accelerates pyroptosis of tubular epithelial cells in sepsis-associated acute kidney injury [2]
Abstract reading summary — source excerpts
- Opening excerpt
- BackgroundLactate accumulation exacerbates the severity of sepsis-associated acute kidney injury (SA-AKI), although the mechanism remains unclear.
- Closing excerpt
- The combined pharmacological strategy of NAD+ supplementation and SPHK1 inhibition represents a promising therapeutic strategy for SA-AKI.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (293 words)
BackgroundLactate accumulation exacerbates the severity of sepsis-associated acute kidney injury (SA-AKI), although the mechanism remains unclear. Since pyroptosis contributes to renal tubular epithelial cell (RTEC) death during SA-AKI, this study explores whether lactate exacerbates pathogenesis by promoting RTEC pyroptosis.MethodsThe clinical correlation between lactate and SA-AKI was examined using the Medical Information Mart for Intensive Care IV (MIMIC-IV) database and patient samples. Lactate's role in RTEC pyroptosis was evaluated in lipopolysaccharide (LPS)-exposed HK-2 cells and in cecal ligation and puncture (CLP)-induced mice. Cross-analyzing bioinformatics and RNA-seq data from LPS/lactate-exposed HK-2 cells revealed pyroptosis genes associated with SA-AKI. Molecular mechanisms were explored via Western blot, ELISA, mitochondrial function assays, chromatin immunoprecipitation (ChIP), and co-immunoprecipitation (co-IP). High-throughput drugs screening was conducted to identify candidates acting on the Sphingosine kinase 1(SPHK1)/Sirtuin 1(SIRT1) axis, which were validated in vitro and in vivo.ResultsLactate aggravated SA-AKI by promoting RTEC pyroptosis. Bioinformatic and functional studies identified SPHK1 as the key mediator. Both SPHK1 knockdown and its inhibitor PF-543 alleviated lactate-augmented pyroptosis. Drug screening identified nicotinamide adenine dinucleotide (NAD+), which simultaneously suppressed SPHK1 expression and the RTEC injury marker kidney injury molecule-1 (KIM-1). Combining NAD+ and PF-543 synergistically attenuated SA-AKI. Sepsis-induced lactate accumulation promoted P300-mediated histone H3 lysine 18 lactylation (H3K18la) at the SPHK1 promoter, epigenetically enhancing its transcription. SPHK1 then phosphorylated and degraded SIRT1, inducing peroxisome proliferator-activated receptor gamma co-activator 1α (PGC-1α) hyperacetylation, thereby impairing SIRT1/PGC-1α signaling and triggering NOD-like receptor family pyrin domain containing 3 (NLRP3) inflammasome-driven pyroptosis. Reciprocally, SIRT1 acted as a delactylase delactylase to reduce H3K18la and inhibit SPHK1 transcription, forming a SPHK1-SIRT1 negative feedback loop.ConclusionsThe study identifies an H3K18la-mediated SPHK1-SIRT1 axis as a key factor of RTEC pyroptosis in SA-AKI. The combined pharmacological strategy of NAD+ supplementation and SPHK1 inhibition represents a promising therapeutic strategy for SA-AKI.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 41799201 · DOI · PMC12964219
Pyroptosis-immune cell cross talk in asthma: From molecular mechanisms to precision therapeutics [3]
Abstract reading summary — source excerpts
- Opening excerpt
- Asthma is a heterogeneous chronic airway disease characterized by complex inflammation.
- Closing excerpt
- By synthesizing these multifaceted roles, this review posits that a nuanced understanding of pyroptosis networks holds significant promise for pioneering endotype-specific therapeutic strategies in asthma management.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (191 words)
Asthma is a heterogeneous chronic airway disease characterized by complex inflammation. Pyroptosis, a pro-inflammatory form of programmed cell death mediated by gasdermin (GSDM) family proteins, has recently emerged as a critical amplifier of airway inflammation and tissue remodeling in asthma. This review delineates the molecular underpinnings of pyroptosis, focusing on the roles of canonical (e.g., NLRP3-caspase-1) and non-canonical (e.g., caspase-4/5/11) inflammasome pathways, as well as the broader concept of PANoptosis. We elaborate on how the pore-forming activity of GSDMD and other GSDMs facilitates the release of potent pro-inflammatory cytokines (IL-1β, IL-18), driving pathogenic cross talk among structural cells (epithelium), innate immune cells (macrophages, eosinophils, ILC2s), and adaptive immunity. Crucially, we contextualize pyroptosis within distinct asthma endotypes, proposing that allergen-driven, NLRP3-dominated pathways may underpin Th2-high/eosinophilic inflammation, while pollutant/viral-triggered, non-canonical/AIM2 pathways may favor Th2-low/neutrophilic phenotypes. The translational potential of targeting pyroptosis is underscored through a discussion of biomarkers (e.g., GSDMD-N, IL-18) and a comprehensive summary of preclinical and early clinical inhibitors targeting NLRP3, GSDMD, and key cytokines. By synthesizing these multifaceted roles, this review posits that a nuanced understanding of pyroptosis networks holds significant promise for pioneering endotype-specific therapeutic strategies in asthma management.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 41394843 · DOI · PMC12698424
Key reviews and meta-analyses
The most cited review-type papers among PubMed’s best-match results for this heading, listed with bibliographic details only. Follow the links for the full text and access terms.
- Research article NLRP3 and pyroptosis blockers for treating inflammatory diseases [4]
- Research article Role of pyroptosis in inflammation and cancer [5]
- Research article Pyroptosis-induced inflammation and tissue damage [6]
- Research article PANoptosis: Mechanisms, biology, and role in disease [7]
- Research article Diversity and complexity of cell death: a historical review [8]
- Research article Dying cells fan the flames of inflammation [9]
References
- Ni FX, Wang HX, Hu J, Chen PS, Huang HJ, Chen HH, et al.. Pyroptosis-driven immune dysregulation in COPD: molecular mechanisms and therapeutic implications. . 2025. PMID 41476973 · DOI · PMC12747962
- Huang Y, Zhao E, Zhao G, Zhuo W, Zhao Y, Wang H, et al.. H3K18 lactylation-mediated SPHK1-SIRT1 feedback loop accelerates pyroptosis of tubular epithelial cells in sepsis-associated acute kidney injury. . 2026. PMID 41799201 · DOI · PMC12964219
- Ni FX, Wang HX, Chen PS, Huang HJ, Chen HH, Huang DH, et al.. Pyroptosis-immune cell cross talk in asthma: From molecular mechanisms to precision therapeutics. . 2025. PMID 41394843 · DOI · PMC12698424
- Coll RC, Schroder K, Pelegrín P. NLRP3 and pyroptosis blockers for treating inflammatory diseases. Trends Pharmacol Sci. 2022. PMID 35513901 · DOI
- Wei X, Xie F, Zhou X, Wu Y, Yan H, Liu T, et al.. Role of pyroptosis in inflammation and cancer. Cell Mol Immunol. 2022. PMID 35970871 · DOI · PMC9376585
- Vasudevan SO, Behl B, Rathinam VA. Pyroptosis-induced inflammation and tissue damage. Semin Immunol. 2023. PMID 37352727 · DOI · PMC10598759
- Sun X, Yang Y, Meng X, Li J, Liu X, Liu H. PANoptosis: Mechanisms, biology, and role in disease. Immunol Rev. 2024. PMID 37823450 · DOI
- Park W, Wei S, Kim BS, Kim B, Bae SJ, Chae YC, et al.. Diversity and complexity of cell death: a historical review. Exp Mol Med. 2023. PMID 37612413 · DOI · PMC10474147
- Newton K, Dixit VM, Kayagaki N. Dying cells fan the flames of inflammation. Science. 2021. PMID 34822265 · DOI
About this article
- Sources
- NLM Medical Subject Headings (definition, synonyms); NCBI PubMed (counts, identifiers); Europe PMC (open-access abstracts and citation counts).
- Verification
- Every reference was resolved against PubMed on 2026-10-31; title, year and DOI matched.
- Review state
- automated source verified; no human expert review has been recorded yet.
- Version
- 1, last updated 2026-10-29.
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Evidence strength
EvidenceHelix's computed view of the study designs behind this topic: how common meta-analyses, randomized trials and reviews are, how recent the literature is, and a plain-language reading. It describes the design mix of the literature. It is not a quality appraisal of any study, and it is not medical advice.