{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,7,23]],"date-time":"2026-07-23T05:03:30Z","timestamp":1784783010634,"version":"3.55.0"},"reference-count":67,"publisher":"Frontiers Media SA","license":[{"start":{"date-parts":[[2026,7,23]],"date-time":"2026-07-23T00:00:00Z","timestamp":1784764800000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":["frontiersin.org"],"crossmark-restriction":true},"short-container-title":["Front. Cardiovasc. Med."],"abstract":"<jats:sec>\n                    <jats:title>Objective<\/jats:title>\n                    <jats:p>Chronic activation of the renin\u2013angiotensin\u2013aldosterone system (RAAS) promotes pathological remodeling of both myocardium and coronary arteries, yet the mechanisms that distinguish myocardial from vascular remodeling remain poorly defined. This study dissected the relative contributions of hemodynamic versus neurohumoral stress to cardiac remodeling, with emphasis on coronary vasculopathy and vascular smooth muscle cell (VSMC) plasticity.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>Three murine models were used: transverse aortic constriction (TAC), angiotensin II (AngII) plus phenylephrine (AngII\/PE), and high-dose angiotensin II (HD-AngII). Hemodynamics were assessed by catheterization at early and late time points. Histological and immunostaining analyses quantified interstitial and perivascular remodeling including cardiomyocyte hypertrophy, interstitial and perivascular fibrosis, VSMC phenotype transitions, proliferation and quiescence markers, and neointimal and elastic lamina remodeling.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>After 28 days, all models exhibited diastolic dysfunction and myocardial fibrosis. Systolic pressure averaged \u223c130 mmHg in both AngII models versus \u223c200 mmHg in TAC. Despite lower pressure, myocardial fibrosis was greater in AngII\/PE and HD AngII models. While TAC induced uniform cardiomyocyte hypertrophy, hypertrophy in AngII models localized near fibrotic and perivascular regions. Increasing AngII dosage shifted remodeling from predominantly myocardial to predominantly vascular phenotypes, accompanied by VSMC dedifferentiation, proliferation, centripetal migration across the internal elastic lamina, neointima formation, elastic lamina disruption, and increased circulating desmosine, consistent with elastin degradation. AKT signaling was selectively increased in coronary VSMCs during this vasculopathic remodeling. Lineage-tracing analyses showed that Ang II\u2013driven coronary neointima formation occurs beneath an intact endothelial monolayer and is composed predominantly of VSMC-derived cells, highlighting a VSMC-centric vasculopathy distinct from classic endothelium-initiated vascular remodeling.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusion<\/jats:title>\n                    <jats:p>Hemodynamic pressure overload and AngII-dominant neurohumoral stress drive distinct cardiac remodeling phenotypes: TAC primarily elicits uniform myocardial hypertrophy and interstitial fibrosis, whereas chronic AngII exposure preferentially promotes a VSMC-centric coronary vasculopathy with perivascular fibrosis and elastic lamina injury at lower pressure load. These complementary models help distinguish pressure-dependent versus AngII-mediated vascular mechanisms and provide a platform to develop targeted therapies for coronary vasculopathy and AngII-driven vascular disease.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.3389\/fcvm.2026.1879443","type":"journal-article","created":{"date-parts":[[2026,7,23]],"date-time":"2026-07-23T04:28:03Z","timestamp":1784780883000},"update-policy":"https:\/\/doi.org\/10.3389\/crossmark-policy","source":"Crossref","is-referenced-by-count":0,"title":["Angiotensin II\u2013driven coronary vasculopathy and pressure-overload myocardial remodeling represent distinct vascular phenotypes"],"prefix":"10.3389","volume":"13","author":[{"given":"Dzmitry","family":"Matsiukevich","sequence":"first","affiliation":[{"name":"Department of Developmental Biology, Washington University in St. Louis School of Medicine","place":["St. Louis, MO, United States"]},{"name":"Department of Pediatrics, Washington University in St. Louis School of Medicine","place":["St. Louis, MO, United States"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"David M.","family":"Ornitz","sequence":"additional","affiliation":[{"name":"Department of Developmental Biology, Washington University in St. Louis School of Medicine","place":["St. Louis, MO, United States"]}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"1965","published-online":{"date-parts":[[2026,7,23]]},"reference":[{"key":"B1","doi-asserted-by":"publisher","first-page":"1696","DOI":"10.1016\/j.jacc.2018.02.021","article-title":"Myocardial interstitial fibrosis in heart failure: biological and translational perspectives","volume":"71","author":"Gonz\u00e1lez","year":"2018","journal-title":"J Am Coll Cardiol"},{"key":"B2","doi-asserted-by":"publisher","first-page":"568","DOI":"10.1172\/JCI31044","article-title":"ECM remodeling in hypertensive heart disease","volume":"117","author":"Berk","year":"2007","journal-title":"J Clin Invest"},{"key":"B3","doi-asserted-by":"publisher","first-page":"1450","DOI":"10.1093\/cvr\/cvaa324","article-title":"Cardiac fibrosis","volume":"117","author":"Frangogiannis","year":"2021","journal-title":"Cardiovasc Res"},{"key":"B4","doi-asserted-by":"publisher","first-page":"e003315","DOI":"10.1161\/CIRCHEARTFAILURE.116.003315","article-title":"Targeting the cardiac myofibroblast secretome to treat myocardial fibrosis in heart failure","volume":"9","author":"Weber","year":"2016","journal-title":"Circ Heart Fail"},{"key":"B5","doi-asserted-by":"publisher","first-page":"631","DOI":"10.1002\/jcp.22322","article-title":"The origin of fibroblasts and mechanism of cardiac fibrosis","volume":"225","author":"Krenning","year":"2010","journal-title":"J Cell Physiol"},{"key":"B6","doi-asserted-by":"publisher","first-page":"549","DOI":"10.1007\/s00018-013-1349-6","article-title":"The pathogenesis of cardiac fibrosis","volume":"71","author":"Kong","year":"2014","journal-title":"Cell Mol Life Sci"},{"key":"B7","doi-asserted-by":"publisher","first-page":"1387","DOI":"10.1161\/01.CIR.82.4.1387","article-title":"Fibrillar collagen and remodeling of dilated canine left ventricle","volume":"82","author":"Weber","year":"1990","journal-title":"Circulation"},{"key":"B8","doi-asserted-by":"publisher","first-page":"1355","DOI":"10.1161\/01.RES.67.6.1355","article-title":"Remodeling of the rat right and left ventricles in experimental hypertension","volume":"67","author":"Brilla","year":"1990","journal-title":"Circ Res"},{"key":"B9","doi-asserted-by":"publisher","first-page":"182","DOI":"10.1016\/j.vph.2012.07.003","article-title":"The role of cardiac fibroblasts in the transition from inflammation to fibrosis following myocardial infarction","volume":"58","author":"Van Nieuwenhoven","year":"2013","journal-title":"Vascul Pharmacol"},{"key":"B10","doi-asserted-by":"publisher","first-page":"107","DOI":"10.1161\/01.RES.69.1.107","article-title":"Impaired diastolic function and coronary reserve in genetic hypertension. 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