{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,7]],"date-time":"2026-10-07T06:52:44Z","timestamp":1791355964175,"version":"4.3.1"},"reference-count":90,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"19","content-domain":{"domain":["www.ahajournals.org"],"crossmark-restriction":true},"short-container-title":["JAHA"],"published-print":{"date-parts":[[2026,10,6]]},"abstract":"<jats:p xml:lang=\"en\">\n                    Recent evidence suggests the\n                    <jats:italic toggle=\"no\">JAK2V617F<\/jats:italic>\n                    mutation may confer an elevated risk of ischemic stroke, likely mediated by systemic inflammation, abnormal cell activation, and endothelial dysfunction. The\n                    <jats:italic toggle=\"no\">JAK2V617F<\/jats:italic>\n                    mutation is an acquired driver mutation reported in up to 11.3% of patients with ischemic stroke in a recent Danish case\u2013control study. It is the main driver mutation in Philadelphia\u2010negative myeloproliferative neoplasms and even in the absence of overt myeloproliferative neoplasm, an increasingly recognized risk factor for cardiovascular disease. In this review, we summarize current knowledge on the biological role of the\n                    <jats:italic toggle=\"no\">JAK2V617F<\/jats:italic>\n                    mutation in thrombosis, its contribution to cerebrovascular risk, and the emerging relevance of\n                    <jats:italic toggle=\"no\">JAK2V617F<\/jats:italic>\n                    in stroke neurology. Current knowledge underscores the value of\n                    <jats:italic toggle=\"no\">JAK2V617F<\/jats:italic>\n                    testing in stroke patients for early detection of myeloproliferative neoplasms or pre\u2013myeloproliferative neoplasm states and personalized secondary stroke prevention. Further studies are needed to refine risk stratification, evaluate targeted interventions, and determine the clinical utility of integrating\n                    <jats:italic toggle=\"no\">JAK2V617F<\/jats:italic>\n                    mutation profiling into stroke care.\n                  <\/jats:p>","DOI":"10.1161\/jaha.126.050497","type":"journal-article","created":{"date-parts":[[2026,9,25]],"date-time":"2026-09-25T04:39:16Z","timestamp":1790311156000},"update-policy":"https:\/\/doi.org\/10.1161\/crossmarkpolicy","source":"Crossref","is-referenced-by-count":0,"title":["<i>JAK2V617F<\/i>\n                    Mutation in Ischemic Stroke: Bridging Hematology and Stroke Neurology"],"prefix":"10.1161","volume":"15","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-4285-6766","authenticated-orcid":false,"given":"Marie H.","family":"Kristiansen","sequence":"first","affiliation":[{"name":"Zealand University Hospital","place":["Roskilde, 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Copenhagen","place":["Denmark"]},{"name":"Zealand University Hospital","place":["Koege, Denmark"]},{"name":"Harvard Medical School","place":["Boston, USA"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-7543-9016","authenticated-orcid":false,"given":"Claus H.","family":"Nielsen","sequence":"additional","affiliation":[{"name":"University of Copenhagen","place":["Denmark"]},{"name":"Copenhagen University Hospital","place":["Copenhagen, Denmark"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-3936-8032","authenticated-orcid":false,"given":"Hans C.","family":"Hasselbalch","sequence":"additional","affiliation":[{"name":"Zealand University Hospital","place":["Roskilde, Denmark"]},{"name":"University of 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