{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,11]],"date-time":"2026-09-11T05:50:02Z","timestamp":1789105802555,"version":"build-2803163510"},"update-to":[{"DOI":"10.1371\/journal.ppat.1012805","type":"new_version","label":"New version","source":"publisher","updated":{"date-parts":[[2024,12,31]],"date-time":"2024-12-31T00:00:00Z","timestamp":1735603200000}}],"reference-count":69,"publisher":"Public Library of Science (PLoS)","issue":"12","license":[{"start":{"date-parts":[[2024,12,17]],"date-time":"2024-12-17T00:00:00Z","timestamp":1734393600000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"funder":[{"DOI":"10.13039\/501100002855","name":"Ministry of Science and Technology of the People's Republic of China","doi-asserted-by":"publisher","award":["2023YFC2306102"],"award-info":[{"award-number":["2023YFC2306102"]}],"id":[{"id":"10.13039\/501100002855","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100002855","name":"Ministry of Science and Technology of the People's Republic of China","doi-asserted-by":"publisher","award":["2019YFA0508500"],"award-info":[{"award-number":["2019YFA0508500"]}],"id":[{"id":"10.13039\/501100002855","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100001809","name":"National Natural Science Foundation of China","doi-asserted-by":"publisher","award":["32130038"],"award-info":[{"award-number":["32130038"]}],"id":[{"id":"10.13039\/501100001809","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["www.plospathogens.org"],"crossmark-restriction":false},"short-container-title":["PLoS Pathog"],"abstract":"<jats:p>\n                    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 Zn\n                    <jats:sup>2+<\/jats:sup>\n                    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.\n                    <jats:italic>SLC30A1<\/jats:italic>\n                    deficiency suppressed multiple inflammasomes by increasing intracellular levels of Zn\n                    <jats:sup>2+<\/jats:sup>\n                    , which bound and inhibited caspase-1 at its active site residues H\n                    <jats:sup>237<\/jats:sup>\n                    , C\n                    <jats:sup>244<\/jats:sup>\n                    and C\n                    <jats:sup>285<\/jats:sup>\n                    . Mutation of these residues almost completely blocked zinc binding. Similarly, Zn\n                    <jats:sup>2+<\/jats:sup>\n                    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\u2019s disease. Thus, zinc might be used to treat inflammasome-related diseases as a broad-spectrum inflammasome inhibitor.\n                  <\/jats:p>","DOI":"10.1371\/journal.ppat.1012805","type":"journal-article","created":{"date-parts":[[2024,12,17]],"date-time":"2024-12-17T13:42:39Z","timestamp":1734442959000},"page":"e1012805","update-policy":"https:\/\/doi.org\/10.1371\/journal.ppat.corrections_policy","source":"Crossref","is-referenced-by-count":22,"title":["Zinc homeostasis regulates caspase activity and inflammasome 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