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However, the direct effect of dsDNA on platelet activation remains unclear. This study aims to investigate the direct influence of dsDNA on platelet activation, thrombosis, and the underlying mechanisms.<\/jats:p>\n               <\/jats:sec>\n               <jats:sec>\n                  <jats:title>Methods and results<\/jats:title>\n                  <jats:p>Analysis of clinical samples revealed elevated plasma dsDNA levels in STEMI patients, which positively correlated with platelet aggregation and markers of neutrophil extracellular traps such as MPO-DNA and CitH3. Platelet assays demonstrated the activation of the cGAS\u2013STING pathway in platelets from STEMI patients. DsDNA directly potentiated platelet activation and thrombus formation. Mechanistic studies using G150 (cGAS inhibitor), H151 (STING inhibitor), and MCC950 (NLRP3 inhibitor), as well as cGAS\u2212\/\u2212, STING\u2212\/\u2212, and NLRP3\u2212\/\u2212 mice, showed that dsDNA activated cGAS, a previously unreported DNA sensor in platelets, and induced activation of the STING\/NLRP3\/caspase-1\/IL-1\u03b2 axis. This cascade enhanced platelet activation and thrombus formation. Platelet cGAS depletion or Palbociclib, a cGAS\u2013STING inhibitor, approved by the FDA for advanced breast cancer, ameliorated myocardial ischaemia-reperfusion injury in ApoE\u2212\/\u2212 mice fed with a high-fat diet for 12 weeks.<\/jats:p>\n               <\/jats:sec>\n               <jats:sec>\n                  <jats:title>Conclusions<\/jats:title>\n                  <jats:p>These results suggested that dsDNA is a novel driver of platelet activation and thrombus formation in STEMI patients.<\/jats:p>\n               <\/jats:sec>","DOI":"10.1093\/cvr\/cvae218","type":"journal-article","created":{"date-parts":[[2024,9,20]],"date-time":"2024-09-20T13:12:43Z","timestamp":1726837963000},"page":"353-366","source":"Crossref","is-referenced-by-count":35,"title":["Double-stranded DNA enhances platelet activation, thrombosis, and myocardial injury via cyclic GMP-AMP 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