{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,13]],"date-time":"2026-10-13T12:43:55Z","timestamp":1791895435869,"version":"4.3.4"},"reference-count":70,"publisher":"Oxford University Press (OUP)","issue":"5","license":[{"start":{"date-parts":[[2022,12,20]],"date-time":"2022-12-20T00:00:00Z","timestamp":1671494400000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/academic.oup.com\/pages\/standard-publication-reuse-rights"}],"funder":[{"name":"Helmholtz Association of German Research Centers","award":["VH-NG-1247"],"award-info":[{"award-number":["VH-NG-1247"]}]},{"DOI":"10.13039\/501100001659","name":"Deutsche Forschungsgemeinschaft","doi-asserted-by":"publisher","id":[{"id":"10.13039\/501100001659","id-type":"DOI","asserted-by":"publisher"}]},{"name":"DFG, German Research Foundation"},{"name":"German Federal Ministry of Education and Research","award":["01KL2005"],"award-info":[{"award-number":["01KL2005"]}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2023,5,22]]},"abstract":"<jats:title>Abstract<\/jats:title>\n               <jats:sec>\n                  <jats:title>Aims<\/jats:title>\n                  <jats:p>Dysregulated immune response contributes to inefficiency of treatment strategies to control hypertension and reduce the risk of end-organ damage. Uncovering the immune pathways driving the transition from the onset of hypertensive stimulus to the manifestation of multi-organ dysfunction are much-needed insights for immune targeted therapy.<\/jats:p>\n               <\/jats:sec>\n               <jats:sec>\n                  <jats:title>Methods and results<\/jats:title>\n                  <jats:p>To aid visualization of cellular events orchestrating multi-organ pathogenesis, we modelled hypertensive cardiovascular remodelling in zebrafish. Zebrafish larvae exposed to ion-poor environment exhibited rapid angiotensinogen up-regulation, followed by manifestation of arterial hypertension and cardiac remodelling that recapitulates key characteristics of incipient heart failure with preserved ejection fraction. In the brain, time-lapse imaging revealed the occurrence of cerebrovascular regression through endothelial retraction and migration in response to the ion-poor treatment. This phenomenon is associated with macrophage\/microglia-endothelial contacts and endothelial junctional retraction. Cytokine and transcriptomic profiling identified systemic up-regulation of interferon-\u03b3 and interleukin 1\u03b2 and revealed altered macrophage\/microglia transcriptional programme characterized by suppression of innate immunity and vasculo\/neuroprotective gene expression. Both zebrafish and a murine model of pressure overload-induced brain damage demonstrated that the brain pathology and macrophage\/microglia phenotypic alteration are dependent on interferon-\u03b3 signalling. In zebrafish, interferon-\u03b3 receptor 1 mutation prevents cerebrovascular remodelling and dysregulation of macrophage\/microglia transcriptomic profile. Supplementation of bone morphogenetic protein 5 identified from the transcriptomic approach as a down-regulated gene in ion-poor-treated macrophages\/microglia that is rescued by interferon-\u03b3 blockage, mitigated cerebral microvessel loss. In mice subjected to transverse aortic constriction-induced pressure overload, typically developing cerebrovascular injury, neuroinflammation, and cognitive dysfunction, interferon-\u03b3 neutralization protected them from blood\u2013brain barrier disruption, cerebrovascular rarefaction, and cognitive decline.<\/jats:p>\n               <\/jats:sec>\n               <jats:sec>\n                  <jats:title>Conclusions<\/jats:title>\n                  <jats:p>These findings uncover cellular and molecular players of an immune pathway communicating hypertensive stimulus to structural and functional remodelling of the brain and identify anti-interferon-\u03b3 treatment as a promising intervention strategy capable of preventing pressure overload-induced damage of the cerebrovascular and nervous systems.<\/jats:p>\n               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