{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,16]],"date-time":"2026-10-16T22:40:01Z","timestamp":1792190401471,"version":"4.4.0"},"reference-count":38,"publisher":"Wiley","issue":"4","license":[{"start":{"date-parts":[[2018,9,24]],"date-time":"2018-09-24T00:00:00Z","timestamp":1537747200000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Journal Cellular Physiology"],"published-print":{"date-parts":[[2019,4]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p>Arecoline induces oral submucous fibrosis (OSF) via promoting the reactive oxygen species (ROS). Angiotensin (1\u20137) (Ang\u2010(1\u20137))\u00a0protects against fibrosis by counteracting angiotensin II (Ang\u2010II) via the Mas receptor. However, the effects of Ang\u2010(1\u20137) on OSF remain unknown. NOD\u2010like receptors (NLRs) family pyrin domain containing 3 (NLRP3) inflammasome is identified as the novel mechanism of fibrosis. Whereas the effects of arecoline on NLRP3 inflammasome remain unclear. We aimed to explore the effect of Ang\u2010(1\u20137) on NLRP3 inflammasome in human oral myofibroblasts. In vivo, activation of NLRP3 inflammasomes with an increase of Ang\u2010II type 1 receptor (AT1R) protein level and ROS production in human oral fibrosis tissues. Ang\u2010(1\u20137) improved arecoline\u2010induced rats OSF, reduced protein levels of NADPH oxidase 4 (NOX4) and the NLRP3 inflammasome. In vitro, arecoline increased ROS along with upregulation of the angiotensin\u2010converting enzyme (ACE)\/Ang\u2010II\/AT1R axis and NLRP3 inflammasome\/interleukin\u20101\u03b2 axis in human oral myofibroblasts, which were reduced by NOX4 inhibitor VAS2870, ROS scavenger <jats:italic>N<\/jats:italic>\u2010acetylcysteine, and NOX4 small interfering RNA (siRNA). Furthermore, arecoline induced collagen synthesis or migration via the Smad or RhoA\u2010ROCK pathway respectively, which could be inhibited by NLRP3 siRNA or caspase\u20101 blocker VX\u2010765. Ang\u2010(1\u20137) shifted the balance of RAS toward the ACE2\/Ang\u2010(1\u20137)\/Mas axis, inhibited arecoline\u2010induced ROS and NLRP3 inflammasome activation, leading to attenuation of migration or collagen synthesis. In summary, Ang\u2010(1\u20137) attenuates arecoline\u2010induced migration and collagen synthesis via inhibiting NLRP3 inflammasome in human oral myofibroblasts.<\/jats:p>","DOI":"10.1002\/jcp.27267","type":"journal-article","created":{"date-parts":[[2018,9,24]],"date-time":"2018-09-24T08:26:06Z","timestamp":1537777566000},"page":"4668-4680","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":43,"title":["Angiotensin (1\u20137) inhibits arecoline\u2010induced migration and collagen synthesis in human oral myofibroblasts via inhibiting NLRP3 inflammasome activation"],"prefix":"10.1002","volume":"234","author":[{"given":"Yuehua","family":"You","sequence":"first","affiliation":[{"name":"Department of Emergency Nanfang Hospital, Southern Medical University Guangzhou China"},{"name":"Department of Stomatology The People\u2019s Hospital of Longhua Shenzhen 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