{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,7]],"date-time":"2026-10-07T18:44:28Z","timestamp":1791398668106,"version":"4.3.3"},"reference-count":29,"publisher":"Wiley","issue":"11","license":[{"start":{"date-parts":[[2026,10,7]],"date-time":"2026-10-07T00:00:00Z","timestamp":1791331200000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"},{"start":{"date-parts":[[2026,10,7]],"date-time":"2026-10-07T00:00:00Z","timestamp":1791331200000},"content-version":"tdm","delay-in-days":0,"URL":"http:\/\/doi.wiley.com\/10.1002\/tdm_license_1.1"}],"funder":[{"DOI":"10.13039\/501100001809","name":"National Natural Science Foundation of China","doi-asserted-by":"publisher","award":["82672068"],"award-info":[{"award-number":["82672068"]}],"id":[{"id":"10.13039\/501100001809","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100001809","name":"National Natural Science Foundation of China","doi-asserted-by":"publisher","award":["82270454"],"award-info":[{"award-number":["82270454"]}],"id":[{"id":"10.13039\/501100001809","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100001809","name":"National Natural Science Foundation of China","doi-asserted-by":"publisher","award":["82670577"],"award-info":[{"award-number":["82670577"]}],"id":[{"id":"10.13039\/501100001809","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100001809","name":"National Natural Science Foundation of China","doi-asserted-by":"publisher","award":["82400449"],"award-info":[{"award-number":["82400449"]}],"id":[{"id":"10.13039\/501100001809","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Acta Physiologica"],"published-print":{"date-parts":[[2026,11]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n                  <jats:p>Immune\u2010inflammatory responses are pivotal regulators of hypertensive vascular remodeling. Specialized pro\u2010resolving mediators (SPMs), including Maresin 2 (MaR2), are endogenous anti\u2010inflammatory molecules. However, the specific role of MaR2 in regulating hypertension and vascular remodeling, as well as its underlying mechanisms, remains unclear. In this study, a murine model of hypertension was induced by continuous infusion of Angiotensin II (AngII) at 1\u2009\u03bcg\/kg\/min. MaR2 intervention (2\u2009\u03bcg\/kg\/day) was administered either prophylactically (before model induction) or therapeutically (after model induction). Prophylactic MaR2 effectively prevented AngII\u2010induced blood pressure elevation and vascular remodeling. Similarly, therapeutic administration after the establishment of hypertension with MaR2 significantly lowered blood pressure and attenuated medial thickening and fibrosis in the aorta and mesenteric arteries. Mechanistic studies revealed that MaR2 significantly inhibited macrophage infiltration and inflammatory responses within vascular tissues. Further in\u00a0vitro and in\u00a0vivo experiments confirmed that MaR2 effectively suppressed AngII\u2010induced macrophage polarization toward a pro\u2010fibrotic phenotype and reduced the acquisition of a myofibroblast\u2010like phenotype (i.e., \u03b1\u2010SMA expression) by macrophages by blocking the TGF\u2010\u03b2\/Smad3 signaling pathway. Notably, pharmacological activation of TGF\u2010\u03b2\/Smad signaling using SRI011381 partially counteracted the protective effects of MaR2 on vascular remodeling. MaR2 attenuates AngII\u2010induced hypertension and vascular remodeling in association with reduced vascular macrophage accumulation and suppression of macrophage pro\u2010fibrotic polarization, at least partly through regulation of TGF\u2010\u03b2\/Smad3 signaling. These findings identify MaR2 as a candidate pro\u2010resolving intervention in an AngII\u2010induced murine model of hypertension and support further mechanistic and translational evaluation in hypertension\u2010associated vascular remodeling.<\/jats:p>","DOI":"10.1111\/apha.70318","type":"journal-article","created":{"date-parts":[[2026,10,7]],"date-time":"2026-10-07T07:39:43Z","timestamp":1791358783000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":1,"title":["Maresin 2 Attenuates Hypertensive Vascular Remodeling via Inhibiting Macrophage Infiltration and Pro\u2010fibrotic Polarization"],"prefix":"10.1111","volume":"242","author":[{"ORCID":"https:\/\/orcid.org\/0000-0001-8630-1725","authenticated-orcid":false,"given":"Shanshan","family":"Peng","sequence":"first","affiliation":[{"name":"Department of Cardiology Renmin Hospital of Wuhan University  Wuhan China"},{"name":"Cardiovascular Research Institute Wuhan University  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