ArticleThe EMBO journal2025
Cardiolipin inhibits the non-canonical inflammasome by preventing LPS binding to caspase-4/11.
Article in The EMBO journal, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
What it found
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Who cites it
11 citing papers in PubMed.
- The gasdermin family: from pyroptosis mechanisms to therapeutic targets.Signal transduction and targeted therapy · 2026Review
- Pyroptosis in chronic obstructive pulmonary disease: Beyond the canonical NLRP3/Caspase-1/GSDMD pathway.Immunologic research · 2026Review
- When folding CARDs wins the game: molecular snapshots of lipopolysaccharide sensing by the non-canonical inflammasome.Biochemical Society transactions · 2026Review
- Innate immunity: current understandings and future perspectives.Signal transduction and targeted therapy · 2026Review
- Kinetic control of macrophage death by PTM-turnover crosstalk in infection and inflammation.Cell chemical biology · 2026Review
- Mitochondrial Dysfunction in Ulcerative Colitis: Pathogenic Mechanisms and Novel Therapeutics.Journal of biochemical and molecular toxicology · 2026Review
- Neuronal inflammasomes: balancing immunity, neuroinflammation, and homeostasis.Trends in immunology · 2026Review
- IL-33 associates with type 2 burden and lung function in paediatric asthma, alongside exploratory IL-33-linked lipid changes.BMC pediatrics · 2026Article
- Neoepitopes at the crossroads of immunometabolism: metabolic remodeling of antigen presentation in type 1 diabetes.Frontiers in immunology · 2026Review
- Molecular mechanisms and regulation of inflammasome activation and signaling: sensing of pathogens and damage molecular patterns.Cellular & molecular immunology · 2025Review
- Cardiolipin's multifaceted role in immune response: a focus on interacting proteins.Frontiers in immunology · 2025Review
Corrections and comments
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Authors and funding
16 authors.
Funding
Abstract
Caspase-4 and caspase-11 (CASP4/11) sense bacterial lipopolysaccharide (LPS). Currently available inhibitors of CASP4/11 also block the activity of caspase-1 (CASP1), which restricts their usefulness in the study of CASP4/11 functions, as well as their clinical potential for the treatment of LPS-linked diseases through CASP4/11 inhibition. Here, we identify mitochondrial cardiolipin as a selective inhibitor of CASP4/11-dependent cell death and inflammatory cytokine secretion, without affecting CASP1 function. Cardiolipin targets the CARD domain of CASP4/11, impeding its interaction with LPS to restrain CASP4/11 activation, thereby suppressing LPS-induced systemic inflammation in vivo. By identifying cardiolipin as a selective inhibitor of CASP4/11, we provide an urgently needed tool for studying caspase-4/11 and noncanonical inflammasome functions in inflammatory pathways and LPS-induced pathogenesis.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.