{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,6]],"date-time":"2026-10-06T15:27:45Z","timestamp":1791300465292,"version":"4.1.0"},"reference-count":24,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"9","content-domain":{"domain":["www.ahajournals.org"],"crossmark-restriction":true},"short-container-title":["ATVB"],"published-print":{"date-parts":[[2013,9]]},"abstract":"<jats:sec>\n                    <jats:title>Objective\u2014<\/jats:title>\n                    <jats:p>Although hypertension is the most common risk factor for thoracic aortic diseases, it is not understood how increased pressures on the ascending aorta lead to aortic aneurysms. We investigated the role of angiotensin II type 1 receptor activation in ascending aortic remodeling in response to increased biomechanical forces using a transverse aortic constriction (TAC) mouse model.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Approach and Results\u2014<\/jats:title>\n                    <jats:p>\n                      Two weeks after TAC, the increased biomechanical pressures led to ascending aortic dilatation and thickening of the medial and adventitial layers of the aorta. There was significant adventitial hyperplasia and inflammatory responses in TAC ascending aortas were accompanied by increased adventitial collagen, elevated inflammatory and proliferative markers, and increased cell density attributable to accumulation of myofibroblasts and macrophages. Treatment with losartan significantly blocked TAC-induced vascular inflammation and macrophage accumulation. However, losartan only partially prevented TAC-induced adventitial hyperplasia, collagen accumulation, and ascending aortic dilatation. Increased\n                      <jats:italic>Tgfb2<\/jats:italic>\n                      expression and phosphorylated-Smad2 staining in the medial layer of TAC ascending aortas were effectively blocked with losartan. In contrast, the increased\n                      <jats:italic>Tgfb1<\/jats:italic>\n                      expression and adventitial phospho-Smad2 staining were only partially attenuated by losartan. In addition, losartan significantly blocked extracellular signal\u2013regulated kinase activation and reactive oxygen species production in the TAC ascending aorta.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions\u2014<\/jats:title>\n                    <jats:p>Inhibition of the angiotensin II type 1 receptor using losartan significantly attenuated the vascular remodeling associated with TAC but did not completely block the increased transforming growth factor-\u03b21 expression, adventitial Smad2 signaling, and collagen accumulation. These results help to delineate the aortic transforming growth factor-\u03b2 signaling that is dependent and independent of the angiotensin II type 1 receptor after TAC.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1161\/atvbaha.113.301624","type":"journal-article","created":{"date-parts":[[2013,7,19]],"date-time":"2013-07-19T00:54:32Z","timestamp":1374195272000},"page":"2172-2179","update-policy":"https:\/\/doi.org\/10.1161\/crossmarkpolicy","source":"Crossref","is-referenced-by-count":79,"title":["Aortic Remodeling After Transverse Aortic Constriction in Mice Is Attenuated With AT\n                    <sub>1<\/sub>\n                    Receptor Blockade"],"prefix":"10.1161","volume":"33","author":[{"given":"Shao-Qing","family":"Kuang","sequence":"first","affiliation":[{"name":"From the Department of Internal Medicine, University of Texas Health Science Center at Houston (S.K., L.G., S.K.P., J.C., S.G., C.V., C.S.K., A.M.P., D.M.M.); and Department of Biochemistry and Molecular Biology, Sealy Center for Molecular Medicine, University of Texas Medical Branch, Galveston (A.R.B.)."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Liang","family":"Geng","sequence":"additional","affiliation":[{"name":"From the Department of Internal Medicine, University of Texas Health Science Center at Houston (S.K., L.G., S.K.P., J.C., S.G., C.V., C.S.K., A.M.P., D.M.M.); and Department of Biochemistry and Molecular Biology, Sealy Center for Molecular Medicine, University of Texas Medical Branch, Galveston (A.R.B.)."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Siddharth K.","family":"Prakash","sequence":"additional","affiliation":[{"name":"From the Department of Internal Medicine, University of Texas Health Science Center at Houston (S.K., L.G., S.K.P., J.C., S.G., C.V., C.S.K., A.M.P., D.M.M.); and Department of Biochemistry and Molecular Biology, Sealy Center for Molecular Medicine, University of Texas Medical Branch, Galveston (A.R.B.)."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jiu-Mei","family":"Cao","sequence":"additional","affiliation":[{"name":"From the Department of Internal Medicine, University of Texas Health Science Center at Houston (S.K., L.G., S.K.P., J.C., S.G., C.V., C.S.K., A.M.P., D.M.M.); and Department of Biochemistry and Molecular Biology, Sealy Center for Molecular Medicine, University of Texas Medical Branch, Galveston (A.R.B.)."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Steven","family":"Guo","sequence":"additional","affiliation":[{"name":"From the Department of Internal Medicine, University of Texas Health Science Center at Houston (S.K., L.G., S.K.P., J.C., S.G., C.V., C.S.K., A.M.P., D.M.M.); and Department of Biochemistry and Molecular Biology, Sealy Center for Molecular Medicine, University of Texas Medical Branch, Galveston (A.R.B.)."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Carlos","family":"Villamizar","sequence":"additional","affiliation":[{"name":"From the Department of Internal Medicine, University of Texas Health Science Center at Houston (S.K., L.G., S.K.P., J.C., S.G., C.V., C.S.K., A.M.P., D.M.M.); and Department of Biochemistry and Molecular Biology, Sealy Center for Molecular Medicine, University of Texas Medical Branch, Galveston (A.R.B.)."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Callie S.","family":"Kwartler","sequence":"additional","affiliation":[{"name":"From the Department of Internal Medicine, University of Texas Health Science Center at Houston (S.K., L.G., S.K.P., J.C., S.G., C.V., C.S.K., A.M.P., D.M.M.); and Department of Biochemistry and Molecular Biology, Sealy Center for Molecular Medicine, University of Texas Medical Branch, Galveston (A.R.B.)."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Andrew M.","family":"Peters","sequence":"additional","affiliation":[{"name":"From the Department of Internal Medicine, University of Texas Health Science Center at Houston (S.K., L.G., S.K.P., J.C., S.G., C.V., C.S.K., A.M.P., D.M.M.); and Department of Biochemistry and Molecular Biology, Sealy Center for Molecular Medicine, University of Texas Medical Branch, Galveston (A.R.B.)."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Allan R.","family":"Brasier","sequence":"additional","affiliation":[{"name":"From the Department of Internal Medicine, University of Texas Health Science Center at Houston (S.K., L.G., S.K.P., J.C., S.G., C.V., C.S.K., A.M.P., D.M.M.); and Department of Biochemistry and Molecular Biology, Sealy Center for Molecular Medicine, University of Texas Medical Branch, Galveston (A.R.B.)."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Dianna M.","family":"Milewicz","sequence":"additional","affiliation":[{"name":"From the Department of Internal Medicine, University of Texas Health Science Center at Houston (S.K., L.G., S.K.P., J.C., S.G., C.V., C.S.K., A.M.P., D.M.M.); and Department of Biochemistry and Molecular Biology, Sealy Center for Molecular Medicine, University of Texas Medical Branch, Galveston (A.R.B.)."}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"276","reference":[{"key":"e_1_3_3_2_2","doi-asserted-by":"publisher","DOI":"10.1161\/CIR.0b013e3181d4739e"},{"key":"e_1_3_3_3_2","doi-asserted-by":"publisher","DOI":"10.1038\/ng.934"},{"key":"e_1_3_3_4_2","doi-asserted-by":"publisher","DOI":"10.1172\/JCI38308"},{"key":"e_1_3_3_5_2","doi-asserted-by":"publisher","DOI":"10.1042\/CS20090372"},{"key":"e_1_3_3_6_2","doi-asserted-by":"publisher","DOI":"10.1159\/000320358"},{"key":"e_1_3_3_7_2","doi-asserted-by":"publisher","DOI":"10.1126\/science.1124287"},{"key":"e_1_3_3_8_2","doi-asserted-by":"publisher","DOI":"10.1172\/JCI44824"},{"key":"e_1_3_3_9_2","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.1202081109"},{"key":"e_1_3_3_10_2","first-page":"1729","article-title":"Transverse aortic constriction in mice.","volume":"38","author":"deAlmeida AC","year":"2010","unstructured":"deAlmeida AC, van Oort RJ, Wehrens XH. 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