{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,6]],"date-time":"2026-10-06T03:51:06Z","timestamp":1791258666435,"version":"4.1.0"},"reference-count":36,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"7","content-domain":{"domain":["www.ahajournals.org"],"crossmark-restriction":true},"short-container-title":["ATVB"],"published-print":{"date-parts":[[2008,7]]},"abstract":"<jats:p>\n            <jats:bold>\n              <jats:italic>Objective\u2014<\/jats:italic>\n            <\/jats:bold>\n            Alpha2-antiplasmin (\u03b12-AP) is the major circulating inhibitor of plasmin, which plays a determining role in the regulation of intravascular fibrinolysis. We investigated the role of \u03b1\n            <jats:sub>2<\/jats:sub>\n            -AP on vascular remodeling in response to angiotensin II (Ang II).\n          <\/jats:p>\n          <jats:p>\n            <jats:bold>\n              <jats:italic>Methods and Results\u2014<\/jats:italic>\n            <\/jats:bold>\n            \u03b12-AP\u2013deficient mice were performed. Ang II and\n            <jats:italic>N<\/jats:italic>\n            <jats:sup>\u03c9<\/jats:sup>\n            -nitro- L-arginine methyl ester (L-NAME)\u2013induced perivascular fibrosis was significantly decreased in \u03b12-AP\n            <jats:sup>\u2212\/\u2212<\/jats:sup>\n            mice compared with wild-type mice. In situ gelatinolytic activity analysis shows that perivascular gelatinolytic activity was increased in \u03b12-AP\n            <jats:sup>\u2212\/\u2212<\/jats:sup>\n            mice, which was responsible for decreased perivascular fibrosis in response to Ang II and L-NAME. Ang II\u2013induced arterial wall thickening, vascular cell proliferation, apoptosis, c-Myc, and collagen \u0399 expression were significantly decreased in \u03b12-AP\n            <jats:sup>\u2212\/\u2212<\/jats:sup>\n            mice compared with wild-type mice. Further analysis shows that increased p53 and p21 expression were responsible for inhibition of Ang II\u2013induced vascular remodeling in \u03b12-AP\n            <jats:sup>\u2212\/\u2212<\/jats:sup>\n            mice.\n          <\/jats:p>\n          <jats:p>\n            <jats:bold>\n              <jats:italic>Conclusion\u2014<\/jats:italic>\n            <\/jats:bold>\n            The results show that \u03b12-AP is a critical regulator for vascular remodeling by inhibiting p53\/p21 pathway, suggesting that \u03b12-AP is proposed to be a potential therapeutic target for vascular remodeling.\n          <\/jats:p>","DOI":"10.1161\/atvbaha.108.165688","type":"journal-article","created":{"date-parts":[[2008,4,25]],"date-time":"2008-04-25T01:37:30Z","timestamp":1209087450000},"page":"1257-1262","update-policy":"https:\/\/doi.org\/10.1161\/crossmarkpolicy","source":"Crossref","is-referenced-by-count":23,"title":["Alpha2-Antiplasmin Is a Critical Regulator of Angiotensin II\u2013Mediated Vascular Remodeling"],"prefix":"10.1161","volume":"28","author":[{"given":"YongZhong","family":"Hou","sequence":"first","affiliation":[{"name":"From the Department of Physiology (Y.Z.H., K.O., C.O., O.M.), Kinki University School of Medicine, Osaka, Japan; and the Department of Food Science and Nutrition (S.U.), Kinki University School of Agriculture, Nara, Japan; and the Department of Microbiology and Infectious Diseases, University of Calgary, Calgary, Alberta T2N 4N1, Canada."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Kiyotaka","family":"Okada","sequence":"additional","affiliation":[{"name":"From the Department of Physiology (Y.Z.H., K.O., C.O., O.M.), Kinki University School of Medicine, Osaka, Japan; and the Department of Food Science and Nutrition (S.U.), Kinki University School of Agriculture, Nara, Japan; and the Department of Microbiology and Infectious Diseases, University of Calgary, Calgary, Alberta T2N 4N1, Canada."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Chikako","family":"Okamoto","sequence":"additional","affiliation":[{"name":"From the Department of Physiology (Y.Z.H., K.O., C.O., O.M.), Kinki University School of Medicine, Osaka, Japan; and the Department of Food Science and Nutrition (S.U.), Kinki University School of Agriculture, Nara, Japan; and the Department of Microbiology and Infectious Diseases, University of Calgary, Calgary, Alberta T2N 4N1, Canada."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Shigeru","family":"Ueshima","sequence":"additional","affiliation":[{"name":"From the Department of Physiology (Y.Z.H., K.O., C.O., O.M.), Kinki University School of Medicine, Osaka, Japan; and the Department of Food Science and Nutrition (S.U.), Kinki University School of Agriculture, Nara, Japan; and the Department of Microbiology and Infectious Diseases, University of Calgary, Calgary, Alberta T2N 4N1, Canada."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Osamu","family":"Matsuo","sequence":"additional","affiliation":[{"name":"From the Department of Physiology (Y.Z.H., K.O., C.O., O.M.), Kinki University School of Medicine, Osaka, Japan; and the Department of Food Science and Nutrition (S.U.), Kinki University School of Agriculture, Nara, Japan; and the Department of Microbiology and Infectious Diseases, University of Calgary, Calgary, Alberta T2N 4N1, Canada."}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"276","reference":[{"key":"e_1_3_3_1_2","first-page":"82","volume":"292","year":"2007","unstructured":"Mehta PK, Griendling KK. 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