{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,7,31]],"date-time":"2026-07-31T14:48:26Z","timestamp":1785509306297,"version":"3.56.0"},"reference-count":49,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"8","content-domain":{"domain":["www.ahajournals.org"],"crossmark-restriction":true},"short-container-title":["JAHA"],"published-print":{"date-parts":[[2026,4,21]]},"abstract":"<jats:sec xml:lang=\"en\">\n                    <jats:title>Background<\/jats:title>\n                    <jats:p xml:lang=\"en\">High salt (HS) intake is a known cardiovascular risk factor, yet the mechanisms linking salt intake to endothelial dysfunction remain unclear. We investigated whether HS induces vascular senescence and dysfunction, and whether targeting senescent cells could prevent these effects.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec xml:lang=\"en\">\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p xml:lang=\"en\">Male C57BL\/6J mice were fed a high\u2010salt diet (HSD [8% NaCl]) for 14 or 28\u2009days. Vascular function was assessed in thoracic aortae and mesenteric arteries using wire myography. Senescence was evaluated by p21, p16, and interleukins (IL) 6 and 1\u03b2 expression in endothelial cells and whole vessels. To test reversibility, mice received the senolytic drug navitoclax.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec xml:lang=\"en\">\n                    <jats:title>Results<\/jats:title>\n                    <jats:p xml:lang=\"en\">A 28\u2010day, but not 14\u2010day, HSD caused endothelial dysfunction and increased vascular senescence markers, indicating senescence. Navitoclax treatment reduced senescence markers, restored vasodilation of mesenteric arteries, and improved vascular contractility. HSD exposure elevated inflammatory gene expression in peritoneal immune cells and increased circulating levels of interleukin\u201016 (IL16). Thus, we treated mesenteric arteries and mesenteric endothelial cells with recombinant IL16 to analyze whether HSD can induce vascular dysfunction via senescence. IL16 caused endothelial dysfunction and increased p21 expression.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec xml:lang=\"en\">\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p xml:lang=\"en\">Prolonged HSD intake induces vascular senescence and dysfunction via immune activation rather than direct endothelial dysfunction, while senolytic therapy prevents HSD\u2010induced vascular dysfunction. Targeting senescence or inflammation, particularly IL16 signaling, may offer new therapeutic strategies for salt\u2010sensitive vascular diseases.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1161\/jaha.125.045304","type":"journal-article","created":{"date-parts":[[2026,4,16]],"date-time":"2026-04-16T11:13:57Z","timestamp":1776338037000},"update-policy":"https:\/\/doi.org\/10.1161\/crossmarkpolicy","source":"Crossref","is-referenced-by-count":2,"title":["High\u2010Salt Diet\u2013Induced Endothelial Dysfunction Is Mediated by Cellular Senescence"],"prefix":"10.1161","volume":"15","author":[{"ORCID":"https:\/\/orcid.org\/0000-0001-6118-2133","authenticated-orcid":false,"given":"Andr\u00e9 F.","family":"Nascimento","sequence":"first","affiliation":[{"name":"University of South Alabama","place":["Mobile, USA"]},{"name":"Federal University of Mato Grosso","place":["Sinop, Brazil"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Renata A. 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