ArticlePLoS pathogens2024
Zinc homeostasis regulates caspase activity and inflammasome activation.
Article in PLoS pathogens, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed.
- Electron-rearranged CuMg@ZIF nanoplatform for pH-Responsive sequential therapy: From infection eradication to neuroangiogenesis in diabetic wounds.Bioactive materials · 2027Article
- AMBRA1 allosterically activates NLRP3 by releasing its autoinhibition.Nature immunology · 2026Article
- Zinc-Containing Bioactive Glass Programs Macrophage Polarization through Extracellular Traps Regulation for Enhanced Diabetic Wound Healing.Advanced healthcare materials · 2026Article
- Metal ions govern coronavirus endoribonuclease activity.Nucleic acids research · 2026Article
- Decoding the molecular mechanisms of pyroptosis and its therapeutic development prospects.Frontiers in cell and developmental biology · 2026Review
- Hydrogel scaffold encapsulating MSC-Exos and ZIF-8 promotes bone regeneration via coordinating osteogenesis and immunomodulation.Bioactive materials · 2025Article
- The protective role of dietary nutrients in mitigating asthma risks induced by indoor air pollutants: a comparative toxicogenomics perspective.Scientific reports · 2025Article
- Article
- Identification of a Four-Gene Signature Based on Metal Metabolism for Alzheimer's Disease Diagnosis.Genes · 2025Article
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Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Inflammasome activation drives pyroptotic cell death and the release of inflammatory cytokines, and many diseases involve its overactivation. Zinc is essential for all organisms as a trace element, but its functions in innate immunity remain undefined. Here, we reported that Zn2+ inhibits caspase-1 to hinder inflammasome activation. We first identified the zinc exporter solute carrier family 30 member 1 (SLC30A1) as an inflammasome regulator, using a genome-wide CRISPR-Cas9-mediated screen. SLC30A1 deficiency suppressed multiple inflammasomes by increasing intracellular levels of Zn2+, which bound and inhibited caspase-1 at its active site residues H237, C244 and C285. Mutation of these residues almost completely blocked zinc binding. Similarly, Zn2+ also inhibited caspase-4/5/11-mediated noncanonical inflammasome activation. Importantly, zinc supplementation significantly relieved cecal ligation and puncture (CLP)-induced sepsis, Imiquimod (IMQ)-induced psoriasis and Alzheimer's disease. Thus, zinc might be used to treat inflammasome-related diseases as a broad-spectrum inflammasome inhibitor.
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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.