{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,26]],"date-time":"2026-09-26T21:41:44Z","timestamp":1790458904675,"version":"4.1.0"},"reference-count":120,"publisher":"Frontiers Media SA","license":[{"start":{"date-parts":[[2022,4,20]],"date-time":"2022-04-20T00:00:00Z","timestamp":1650412800000},"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. Pharmacol."],"abstract":"<jats:p>Transforming growth factor-beta (TGF-\u03b2) signaling is essential for the maintenance of the normal structure and function of the aorta. It includes SMAD-dependent canonical pathways and noncanonical signaling pathways. Accumulated genetic evidence has shown that TGF-\u03b2 canonical signaling-related genes have key roles in aortic aneurysms (AAs) and aortic dissections and many gene mutations have been identified in patients, such as those for transforming growth factor-beta receptor one TGFBR1, TGFBR2, SMAD2, SMAD3, SMAD4, and SMAD6. Aortic specimens from patients with these mutations often show paradoxically enhanced TGF-\u03b2 signaling. Some hypotheses have been proposed and new AA models in mice have been constructed to reveal new mechanisms, but the role of TGF-\u03b2 signaling in AAs is controversial. In this review, we focus mainly on the role of canonical signaling-related core genes in diseases of the aorta, as well as recent advances in gene-mutation detection, animal models, and <jats:italic>in vitro<\/jats:italic> studies.<\/jats:p>","DOI":"10.3389\/fphar.2022.888563","type":"journal-article","created":{"date-parts":[[2022,4,20]],"date-time":"2022-04-20T05:58:38Z","timestamp":1650434318000},"update-policy":"https:\/\/doi.org\/10.3389\/crossmark-policy","source":"Crossref","is-referenced-by-count":31,"title":["Association of TGF-\u03b2 Canonical Signaling-Related Core Genes With Aortic Aneurysms and Aortic Dissections"],"prefix":"10.3389","volume":"13","author":[{"given":"Jicheng","family":"Chen","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Rong","family":"Chang","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"1965","published-online":{"date-parts":[[2022,4,20]]},"reference":[{"key":"B1","doi-asserted-by":"publisher","first-page":"1165","DOI":"10.1002\/ajmg.a.33968","article-title":"SMAD4 Mutation Segregating in a Family with Juvenile Polyposis, Aortopathy, and Mitral Valve Dysfunction","author":"Andrabi","year":"2011","journal-title":"Am. 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