{"id":63193,"date":"2022-11-09T11:38:53","date_gmt":"2022-11-09T10:38:53","guid":{"rendered":"https:\/\/cri1149.fr\/?post_type=publications&#038;p=63193"},"modified":"2025-09-11T16:47:59","modified_gmt":"2025-09-11T14:47:59","slug":"jak2v617f-mutation-drives-vascular-resident-macrophages-toward-a-pathogenic-phenotype-and-promotes-dissecting-aortic-aneurysm","status":"publish","type":"publication","link":"https:\/\/cri1149.fr\/en\/publication\/jak2v617f-mutation-drives-vascular-resident-macrophages-toward-a-pathogenic-phenotype-and-promotes-dissecting-aortic-aneurysm\/","title":{"rendered":"JAK2V617F mutation drives vascular resident macrophages toward a pathogenic phenotype and promotes dissecting aortic aneurysm"},"content":{"rendered":"","protected":false},"featured_media":0,"template":"","meta":{"_acf_changed":false,"_EventAllDay":false,"_EventTimezone":"","_EventStartDate":"","_EventEndDate":"","_EventStartDateUTC":"","_EventEndDateUTC":"","_EventShowMap":false,"_EventShowMapLink":false,"_EventURL":"","_EventCost":"","_EventCostDescription":"","_EventCurrencySymbol":"","_EventCurrencyCode":"","_EventCurrencyPosition":"","_EventDateTimeSeparator":"","_EventTimeRangeSeparator":"","_EventOrganizerID":[],"_EventVenueID":[],"_OrganizerEmail":"","_OrganizerPhone":"","_OrganizerWebsite":"","_VenueAddress":"","_VenueCity":"","_VenueCountry":"","_VenueProvince":"","_VenueState":"","_VenueZip":"","_VenuePhone":"","_VenueURL":"","_VenueStateProvince":"","_VenueLat":"","_VenueLng":"","_VenueShowMap":false,"_VenueShowMapLink":false},"category_publication":[],"class_list":["post-63193","publication","type-publication","status-publish","hentry"],"acf":{"numero_de_publication":"[:fr]Nature Communications.[:]","date_de_publication":"20221103","numero_doi":"","equipe":[166],"auteurs-liste":[{"texte_libre":true,"auteur-lien":null,"auteur-text":"[:fr]Rida Al-Rifai[:]"},{"texte_libre":true,"auteur-lien":null,"auteur-text":"[:fr]Marie Vandestienne[:]"},{"texte_libre":true,"auteur-lien":null,"auteur-text":"[:fr]Jean-R\u00e9mi Lavillegrand[:]"},{"texte_libre":true,"auteur-lien":null,"auteur-text":"[:fr]Tristan Mirault[:]"},{"texte_libre":true,"auteur-lien":null,"auteur-text":"[:fr]Julie Cornebise[:]"},{"texte_libre":false,"auteur-lien":13246,"auteur-text":""},{"texte_libre":true,"auteur-lien":null,"auteur-text":"[:fr]Ludivine Laurans[:]"},{"texte_libre":true,"auteur-lien":null,"auteur-text":"[:fr]Bruno Esposito[:]"},{"texte_libre":true,"auteur-lien":null,"auteur-text":"[:fr]Chlo\u00e9 James[:]"},{"texte_libre":true,"auteur-lien":null,"auteur-text":"[:fr]Olivier Mansier[:]"},{"texte_libre":true,"auteur-lien":null,"auteur-text":"[:fr]Pierre Hirsch[:]"},{"texte_libre":true,"auteur-lien":null,"auteur-text":"[:fr]Fabrizia Favale[:]"},{"texte_libre":true,"auteur-lien":null,"auteur-text":"[:fr]Rayan Braik[:]"},{"texte_libre":true,"auteur-lien":null,"auteur-text":"[:fr]Camille Knosp[:]"},{"texte_libre":true,"auteur-lien":null,"auteur-text":"[:fr]Jose Vilar[:]"},{"texte_libre":true,"auteur-lien":null,"auteur-text":"[:fr]Giuseppe Rizzo[:]"},{"texte_libre":true,"auteur-lien":null,"auteur-text":"[:fr]Alma Zernecke[:]"},{"texte_libre":true,"auteur-lien":null,"auteur-text":"[:fr]Antoine-Emmanuel Saliba[:]"},{"texte_libre":true,"auteur-lien":null,"auteur-text":"[:fr]Alain Tedgui[:]"},{"texte_libre":true,"auteur-lien":null,"auteur-text":"[:fr]Maxime Lacroix[:]"},{"texte_libre":true,"auteur-lien":null,"auteur-text":"[:fr]Lionel Arrive[:]"},{"texte_libre":true,"auteur-lien":null,"auteur-text":"[:fr]Ziad Mallat[:]"},{"texte_libre":true,"auteur-lien":null,"auteur-text":"[:fr]Soraya Taleb[:]"},{"texte_libre":true,"auteur-lien":null,"auteur-text":"[:fr]Marc Diedisheim[:]"},{"texte_libre":true,"auteur-lien":null,"auteur-text":"[:fr]Cl\u00e9ment Cochain[:]"},{"texte_libre":false,"auteur-lien":13244,"auteur-text":""},{"texte_libre":true,"auteur-lien":null,"auteur-text":"[:fr]Hafid Ait-Oufella[:]"}],"auteurs-manuel":"","liens_externes":null,"liens":[{"lien":"https:\/\/www.nature.com\/articles\/s41467-022-34469-1"}],"paragraphe":"<h2 id=\"Abs1\" class=\"c-article-section__title js-section-title js-c-reading-companion-sections-item\" style=\"text-align: justify;\">Abstract<\/h2>\r\n<div id=\"Abs1-content\" class=\"c-article-section__content\">\r\n<p style=\"text-align: justify;\">JAK2V617F mutation is associated with an increased risk for athero-thrombotic cardiovascular disease, but its role in aortic disease development and complications remains unknown. In a cohort of patients with myeloproliferative neoplasm,\u00a0<i>JAK2V617F<\/i>\u00a0mutation was identified as an independent risk factor for dilation of both the ascending and descending thoracic aorta. Using single-cell RNA-seq, complementary genetically-modified mouse models, as well as pharmacological approaches, we found that\u00a0<i>JAK2V617F<\/i>\u00a0mutation was associated with a pathogenic pro-inflammatory phenotype of perivascular tissue-resident macrophages, which promoted deleterious aortic wall remodeling at early stages, and dissecting aneurysm through the recruitment of circulating monocytes at later stages. Finally, genetic manipulation of tissue-resident macrophages, or treatment with a Jak2 inhibitor, ruxolitinib, mitigated aortic wall inflammation and reduced aortic dilation and rupture. Overall,\u00a0<i>JAK2V617F<\/i>\u00a0mutation drives vascular resident macrophages toward a pathogenic phenotype and promotes dissecting aortic aneurysm.<\/p>\r\n<\/div>","paragraphe_en":"<h2 id=\"Abs1\" class=\"c-article-section__title js-section-title js-c-reading-companion-sections-item\" style=\"text-align: justify;\">Abstract<\/h2>\r\n<div id=\"Abs1-content\" class=\"c-article-section__content\">\r\n<p style=\"text-align: justify;\">JAK2V617F mutation is associated with an increased risk for athero-thrombotic cardiovascular disease, but its role in aortic disease development and complications remains unknown. In a cohort of patients with myeloproliferative neoplasm,\u00a0<i>JAK2V617F<\/i>\u00a0mutation was identified as an independent risk factor for dilation of both the ascending and descending thoracic aorta. Using single-cell RNA-seq, complementary genetically-modified mouse models, as well as pharmacological approaches, we found that\u00a0<i>JAK2V617F<\/i>\u00a0mutation was associated with a pathogenic pro-inflammatory phenotype of perivascular tissue-resident macrophages, which promoted deleterious aortic wall remodeling at early stages, and dissecting aneurysm through the recruitment of circulating monocytes at later stages. Finally, genetic manipulation of tissue-resident macrophages, or treatment with a Jak2 inhibitor, ruxolitinib, mitigated aortic wall inflammation and reduced aortic dilation and rupture. Overall,\u00a0<i>JAK2V617F<\/i>\u00a0mutation drives vascular resident macrophages toward a pathogenic phenotype and promotes dissecting aortic aneurysm.<\/p>\r\n<\/div>","documents":null},"yoast_head":"<!-- This site is optimized with the Yoast SEO plugin v27.4 - https:\/\/yoast.com\/product\/yoast-seo-wordpress\/ -->\n<title>JAK2V617F mutation drives vascular resident macrophages toward a pathogenic phenotype and promotes dissecting aortic aneurysm - CRI<\/title>\n<meta name=\"robots\" content=\"index, follow, max-snippet:-1, max-image-preview:large, max-video-preview:-1\" \/>\n<link rel=\"canonical\" href=\"https:\/\/cri1149.fr\/publication\/jak2v617f-mutation-drives-vascular-resident-macrophages-toward-a-pathogenic-phenotype-and-promotes-dissecting-aortic-aneurysm\/\" \/>\n<meta property=\"og:locale\" content=\"en_US\" \/>\n<meta property=\"og:type\" content=\"article\" \/>\n<meta property=\"og:title\" content=\"JAK2V617F mutation drives vascular resident macrophages toward a pathogenic phenotype and promotes dissecting aortic aneurysm - 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