{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,10]],"date-time":"2026-10-10T11:53:39Z","timestamp":1791633219395,"version":"4.3.4"},"reference-count":50,"publisher":"Ovid Technologies (Wolters Kluwer Health)","content-domain":{"domain":["www.ahajournals.org"],"crossmark-restriction":true},"short-container-title":["JAHA"],"abstract":"<jats:sec xml:lang=\"en\">\n                    <jats:title>Background<\/jats:title>\n                    <jats:p xml:lang=\"en\">Thoracic aortic dissection (TAD) is a life\u2010threatening vascular disease that lacks effective pharmacological treatment. Canonical transient receptor potential (TRPC) channels are involved in regulating various cardiovascular functions, yet their roles in TAD have not been elucidated.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec xml:lang=\"en\">\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p xml:lang=\"en\">Three\u2010week\u2010old male mice were administered \u03b2\u2010aminopropionitrile dissolved in drinking water for 28\u2009days to induce TAD formation. The effects of TRPCs on TAD were explored in\u00a0vitro and in\u00a0vivo. RNA sequencing of thoracic aortas was performed to investigate the mechanism by which TRPCs regulate TAD progression.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec xml:lang=\"en\">\n                    <jats:title>Results<\/jats:title>\n                    <jats:p xml:lang=\"en\">\n                      Among the TRPC family members, TRPC1 expression was markedly increased in aortas from \u03b2\u2010aminopropionitrile\u2013induced TAD mice along with the downregulation of the vascular smooth muscle cell (SMC) contractile markers smooth muscle \u03b1\u2010actin and smooth muscle 22. Compared with control littermates, SMC\u2010specific\n                      <jats:italic toggle=\"yes\">TRPC1<\/jats:italic>\n                      deficiency in mice alleviated \u03b2\u2010aminopropionitrile\u2013induced TAD formation characterized by decreased aortic rupture, reduced maximal thoracic aortic diameters, and less elastin degradation. Conversely, SMC\u2010specific knock\u2010in of\n                      <jats:italic toggle=\"no\">TRPC1<\/jats:italic>\n                      exacerbated TAD development in mice. Unbiased RNA sequencing showed that\n                      <jats:italic toggle=\"no\">TRPC1<\/jats:italic>\n                      knockout in vascular SMCs inhibited the expression of inflammatory factors and chemokines in thoracic aortas during the early stage of \u03b2\u2010aminopropionitrile administration. Mechanistically, TRPC1 induced the proinflammatory phenotypic transition of vascular SMCs by activating the calcineurin\/nuclear factor\u2010\u03baB pathway, thereby contributing to vascular inflammation and TAD development.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec xml:lang=\"en\">\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p xml:lang=\"en\">Our study identified TRPC1 as a novel endogenous pathogenic factor for vascular SMC inflammatory phenotypic transition and TAD formation and provided new insights for a comprehensive understanding of the mechanisms during TAD. Blocking the TRPC1\/calcineurin\/nuclear factor\u2010\u03baB signaling suppressed TAD progression, which may be a promising strategy to address TAD.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1161\/jaha.126.048571","type":"journal-article","created":{"date-parts":[[2026,10,10]],"date-time":"2026-10-10T11:46:22Z","timestamp":1791632782000},"update-policy":"https:\/\/doi.org\/10.1161\/crossmarkpolicy","source":"Crossref","is-referenced-by-count":0,"title":["TRPC1 Promotes Thoracic Aortic Dissection Through Inducing Proinflammatory Phenotype of Vascular Smooth Muscle Cells"],"prefix":"10.1161","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-0169-7471","authenticated-orcid":false,"given":"Liu","family":"Yang","sequence":"first","affiliation":[{"name":"Jiangnan University","place":["Wuxi, China"]},{"name":"Jiangnan University","place":["Wuxi, 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