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Our previous studies found that activating \u03b17 nicotinic acetylcholine receptor (\u03b17nAChR) had a protective effect on vascular injury. This work was to investigate whether activating \u03b17nAChR could influence AAA formation and explore its mechanisms. AAA models were established by angiotensin II (Ang II) infusion in ApoE\n                    <jats:sup>\u2212<\/jats:sup>\n                    <jats:sup>\/\u2212<\/jats:sup>\n                    mice or in wild type and \u03b17nAChR\n                    <jats:sup>\u2212\/\u2212<\/jats:sup>\n                    mice. In vitro mouse aortic smooth muscle (MOVAS) cells were treated with tumor necrosis factor-\u03b1 (TNF-\u03b1). PNU-282987 was chosen to activate \u03b17nAChR. We found that cell pyroptosis effector GSDMD and NLRP3 inflammasome were activated in abdominal aorta, and inflammatory cytokines in serum were elevated in AAA models of ApoE\n                    <jats:sup>\u2212\/\u2212<\/jats:sup>\n                    mice. Activating \u03b17nAChR reduced maximal aortic diameters, preserved elastin integrity and decreased inflammatory responses in ApoE\n                    <jats:sup>\u2212\/\u2212<\/jats:sup>\n                    mice with Ang II infusion. While \u03b17nAChR\n                    <jats:sup>\u2212\/\u2212<\/jats:sup>\n                    mice led to aggravated aortic injury and increased inflammatory cytokines with Ang II infusion when compared with wild type. Moreover, activating \u03b17nAChR inhibited NLRP3\/caspase-1\/GSDMD pathway in AAA model of ApoE\n                    <jats:sup>\u2212\/\u2212<\/jats:sup>\n                    mice, while \u03b17nAChR deficiency promoted this pathway. In vitro, N-acetylcysteine (NAC) inhibited NLRP3 inflammasome activation and NLRP3 knockdown reduced GSDMD expression, in MOVAS cells\u00a0treated with TNF-\u03b1. Furthermore, activating \u03b17nAChR inhibited oxidative stress, reduced NLRP3\/GSDMD expression, and decreased cell pyroptosis in MOVAS cells\u00a0with TNF-\u03b1. In conclusion, our study found that activating \u03b17nAChR retarded AAA through inhibiting pyroptosis mediated by NLRP3 inflammasome. These suggested that \u03b17nAChR would be a potential pharmacological target for AAA.\n                  <\/jats:p>","DOI":"10.1038\/s41401-022-00876-9","type":"journal-article","created":{"date-parts":[[2022,2,25]],"date-time":"2022-02-25T07:03:34Z","timestamp":1645772614000},"page":"2585-2595","update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":52,"title":["Activating \u03b17nAChR ameliorates abdominal aortic aneurysm through inhibiting pyroptosis mediated by NLRP3 inflammasome"],"prefix":"10.1038","volume":"43","author":[{"given":"Hui","family":"Fu","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Qi-rui","family":"Shen","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yi","family":"Zhao","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Min","family":"Ni","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Can-can","family":"Zhou","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ji-kuai","family":"Chen","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Chen","family":"Chi","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Dong-jie","family":"Li","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Guang","family":"Liang","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Fu-ming","family":"Shen","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"297","published-online":{"date-parts":[[2022,2,25]]},"reference":[{"key":"876_CR1","doi-asserted-by":"publisher","first-page":"799","DOI":"10.1161\/CIRCRESAHA.116.310367","volume":"120","author":"D Ma","year":"2017","unstructured":"Ma D, Zheng B, Suzuki T, Zhang R, Jiang C, Bai D, et al. 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