{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,27]],"date-time":"2026-10-27T01:16:28Z","timestamp":1793063788551,"version":"4.5.0"},"reference-count":90,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"6","content-domain":{"domain":["www.ahajournals.org"],"crossmark-restriction":true},"short-container-title":["JAHA"],"published-print":{"date-parts":[[2026,3,17]]},"abstract":"<jats:sec xml:lang=\"en\">\n                    <jats:title>Background<\/jats:title>\n                    <jats:p xml:lang=\"en\">Ischemic stroke remains a leading cause of morbidity and mortality worldwide, with limited treatment options available. Vascular dysfunction is a key pathomechanism, and brain endothelial cells (bECs) play a critical role in determining stroke outcomes. This study investigates the specific roles of YAP (yes\u2010associated protein 1) and TAZ (WW domain containing transcription regulator 1) in regulating bEC functions during stroke.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec xml:lang=\"en\">\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p xml:lang=\"en\">\n                      Mice underwent 30\u2010minute middle cerebral artery occlusion (MCAo) followed by reperfusion to model ischemic stroke. TAZ reporter mice were used to track stroke\u2010induced subcellular changes in TAZ expression. Tamoxifen\u2010inducible endothelial\u2010specific\n                      <jats:italic toggle=\"yes\">Yap<\/jats:italic>\n                      \/\n                      <jats:italic toggle=\"yes\">Taz<\/jats:italic>\n                      knockout and control mice were used to study YAP\/TAZ\u2019s role in bEC function post\u2010stroke. Stroke outcomes were measured by magnetic resonance imaging and NeuN (neuronal nuclei)\u2010associated lesion analysis. Properties of bECs were assessed via immunohistochemistry and RNA sequencing. Inflammatory parameters were analyzed by flow cytometry of brain immune cells and quantitative polymerase chain reaction.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec xml:lang=\"en\">\n                    <jats:title>Results<\/jats:title>\n                    <jats:p xml:lang=\"en\">\n                      Middle cerebral artery occlusion\/reperfusion regulated\n                      <jats:italic toggle=\"no\">Yap<\/jats:italic>\n                      ,\n                      <jats:italic toggle=\"no\">Taz<\/jats:italic>\n                      , and YAP\/TAZ target gene expression in the brain. TAZ reporter mice confirmed stroke\u2010induced endothelial YAP\/TAZ activation. Endothelial\u2010specific loss of YAP\/TAZ reduced infarct volumes at 4\u2009weeks after MCAo without impairing stroke\u2010induced angiogenesis, revealing an unexpected neuroprotective role for endothelial YAP\/TAZ depletion. YAP\/TAZ deficiency modulated cGAS\u2212STING (cyclic GMP\u2010AMP synthase\u2212stimulator of interferon genes) and Wnt (wingless\u2010related integration site) signaling genes in bECs and promoted myeloid cell recruitment and an anti\u2010inflammatory vascular environment during the subacute phase of stroke.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec xml:lang=\"en\">\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p xml:lang=\"en\">Our data suggest that endothelial YAP\/TAZ affects the inflammatory milieu subacutely after ischemia and thereby influences the chronic course of stroke. Modulation of YAP\/TAZ activity in ECs may be a promising therapeutic target to promote neuroprotection after stroke.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1161\/jaha.124.040079","type":"journal-article","created":{"date-parts":[[2025,11,26]],"date-time":"2025-11-26T12:26:13Z","timestamp":1764159973000},"update-policy":"https:\/\/doi.org\/10.1161\/crossmarkpolicy","source":"Crossref","is-referenced-by-count":6,"title":["Loss of Endothelial YAP\/TAZ Reduces the Size of Chronic Stroke Lesions and Alters the Endothelial Environment"],"prefix":"10.1161","volume":"15","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-4756-7381","authenticated-orcid":false,"given":"Ria","family":"G\u00f6ttert","sequence":"first","affiliation":[{"name":"Charit\u00e9\u2014Universit\u00e4tsmedizin Berlin, Corporate Member of Freie Universit\u00e4t Berlin, Humboldt\u2010Universit\u00e4t zu Berlin, and Berlin Institute of Health, Klinik f\u00fcr Neurologie und Abteilung f\u00fcr Experimentelle 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