{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,30]],"date-time":"2026-09-30T04:11:58Z","timestamp":1790741518281,"version":"4.1.0"},"reference-count":58,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"4","content-domain":{"domain":["www.ahajournals.org"],"crossmark-restriction":true},"short-container-title":["Circulation Research"],"published-print":{"date-parts":[[2024,8,2]]},"abstract":"<jats:sec>\n            <jats:title>BACKGROUND:<\/jats:title>\n            <jats:p>The long isoform of the Wnk1 (with-no-lysine [K] kinase 1) is a ubiquitous serine\/threonine kinase, but its role in vascular smooth muscle cells (VSMCs) pathophysiology remains unknown.<\/jats:p>\n          <\/jats:sec>\n          <jats:sec>\n            <jats:title>METHODS:<\/jats:title>\n            <jats:p>\n              AngII (angiotensin II) was infused in\n              <jats:italic toggle=\"yes\">\n                Apoe\n                <jats:sup>\u2212\/\u2212<\/jats:sup>\n              <\/jats:italic>\n              to induce experimental aortic aneurysm. Mice carrying an\n              <jats:italic toggle=\"yes\">Sm22-Cre<\/jats:italic>\n              allele were cross-bred with mice carrying a floxed\n              <jats:italic toggle=\"yes\">Wnk1<\/jats:italic>\n              allele to specifically investigate the functional role of Wnk1 in VSMCs.\n            <\/jats:p>\n          <\/jats:sec>\n          <jats:sec>\n            <jats:title>RESULTS:<\/jats:title>\n            <jats:p>\n              Single-cell RNA-sequencing of the aneurysmal abdominal aorta from AngII-infused\n              <jats:italic toggle=\"yes\">\n                Apoe\n                <jats:sup>\u2212\/\u2212<\/jats:sup>\n              <\/jats:italic>\n              mice revealed that VSMCs that did not express Wnk1 showed lower expression of contractile phenotype markers and increased inflammatory activity. Interestingly, WNK1 gene expression in VSMCs was decreased in human abdominal aortic aneurysm.\n              <jats:italic toggle=\"yes\">Wnk1<\/jats:italic>\n              -deficient VSMCs lost their contractile function and exhibited a proinflammatory phenotype, characterized by the production of matrix metalloproteases, as well as cytokines and chemokines, which contributed to local accumulation of inflammatory macrophages, Ly6C\n              <jats:sup>hi<\/jats:sup>\n              monocytes, and \u03b3\u03b4 T cells.\n              <jats:italic toggle=\"yes\">Sm22Cre+Wnk1<\/jats:italic>\n              <jats:sup>\n                <jats:italic toggle=\"yes\">lox\/lox<\/jats:italic>\n              <\/jats:sup>\n              mice spontaneously developed aortitis in the infrarenal abdominal aorta, which extended to the thoracic area over time without any negative effect on long-term survival. AngII infusion in\n              <jats:italic toggle=\"yes\">Sm22Cre+Wnk1<\/jats:italic>\n              <jats:sup>\n                <jats:italic toggle=\"yes\">lox\/lox<\/jats:italic>\n              <\/jats:sup>\n              mice aggravated the aortic disease, with the formation of lethal abdominal aortic aneurysms. Pharmacological blockade of \u03b3\u03b4 T-cell recruitment using neutralizing anti-CXCL9 (anti-CXC motif chemokine ligand 9) antibody treatment, or of monocyte\/macrophage using Ki20227, a selective inhibitor of CSF1 receptor, attenuated aortitis.\n              <jats:italic toggle=\"yes\">Wnk1<\/jats:italic>\n              deletion in VSMCs led to aortic wall remodeling with destruction of elastin layers, increased collagen content, and enhanced local TGF-\u03b2 (transforming growth factor-beta) 1 expression. Finally, in vivo TGF-\u03b2 blockade using neutralizing anti-TGF-\u03b2 antibody promoted saccular aneurysm formation and aorta rupture in\n              <jats:italic toggle=\"yes\">Sm22 Cre+ Wnk1<\/jats:italic>\n              <jats:sup>\n                <jats:italic toggle=\"yes\">lox\/lox<\/jats:italic>\n              <\/jats:sup>\n              mice but not in control animals.\n            <\/jats:p>\n          <\/jats:sec>\n          <jats:sec>\n            <jats:title>CONCLUSION:<\/jats:title>\n            <jats:p>\n              Wnk1 is a key regulator of VSMC function.\n              <jats:italic toggle=\"yes\">Wnk1<\/jats:italic>\n              deletion promotes VSMC phenotype switch toward a pathogenic proinflammatory phenotype, orchestrating deleterious vascular remodeling and spontaneous severe aortitis in mice.\n            <\/jats:p>\n          <\/jats:sec>","DOI":"10.1161\/circresaha.124.324366","type":"journal-article","created":{"date-parts":[[2024,7,9]],"date-time":"2024-07-09T09:01:12Z","timestamp":1720515672000},"page":"488-502","update-policy":"https:\/\/doi.org\/10.1161\/crossmarkpolicy","source":"Crossref","is-referenced-by-count":13,"title":["L-Wnk1 Deletion in Smooth Muscle Cells Causes Aortitis and Inflammatory Shift"],"prefix":"10.1161","volume":"135","author":[{"ORCID":"https:\/\/orcid.org\/0009-0003-5079-7943","authenticated-orcid":true,"given":"Helene","family":"Quelquejay","sequence":"first","affiliation":[{"name":"Universit\u00e9 de Paris, Inserm U970, Paris-Cardiovascular Research Center, France (H.Q., R.A.-R., M.V., I.F., T.M., X.Z., I.S.-Z., G.G., P.A., E.R., G.A., D.B., S.T., A.T., C.M.B., S.B., X.J., 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