{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,10]],"date-time":"2026-09-10T20:40:34Z","timestamp":1789072834287,"version":"build-2803163510"},"reference-count":63,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"7","content-domain":{"domain":["www.ahajournals.org"],"crossmark-restriction":true},"short-container-title":["ATVB"],"published-print":{"date-parts":[[2019,7]]},"abstract":"<jats:sec>\n            <jats:title>Objective\u2014<\/jats:title>\n            <jats:p>Inhibition of SIRT (sirtuin)-1, a nicotinamide adenine dinucleotide-dependent protein deacetylase, is linked to cigarette smoking-induced arterial stiffness, but the underlying mechanisms remain largely unknown. The aim of the present study was to determine the effects and mechanisms of nicotine, a major component of cigarette smoke, on SIRT1 activity and arterial stiffness.<\/jats:p>\n          <\/jats:sec>\n          <jats:sec>\n            <jats:title>Approach and Results\u2014<\/jats:title>\n            <jats:p>\n              Arterial stiffness, peroxynitrite (ONOO\n              <jats:sup>\u2212<\/jats:sup>\n              ) formation, SIRT1 expression and activity were monitored in mouse aortas of 8-week-old C57BL\/6 mice (wild-type) or\n              <jats:italic>Sirt1<\/jats:italic>\n              -overexpressing (\n              <jats:italic>Sirt1<\/jats:italic>\n              <jats:sup>\n                <jats:italic>Super<\/jats:italic>\n              <\/jats:sup>\n              ) mice with or without nicotine for 4 weeks. In aortas of wild-type mice, nicotine reduced SIRT1 protein and activity by \u224850% without affecting its mRNA levels. In those from\n              <jats:italic>Sirt1<\/jats:italic>\n              <jats:sup>\n                <jats:italic>Super<\/jats:italic>\n              <\/jats:sup>\n              mice, nicotine also markedly reduced SIRT1 protein and activity to the levels that were comparable to those in wild-type mice. Nicotine infusion significantly induced collagen I, fibronectin, and arterial stiffness in wild-type but not\n              <jats:italic>Sirt1<\/jats:italic>\n              <jats:sup>\n                <jats:italic>Super<\/jats:italic>\n              <\/jats:sup>\n              mice. Nicotine increased the levels of iNOS (inducible nitric oxide synthase) and the co-staining of SIRT1 and 3-nitrotyrosine, a footprint of ONOO\n              <jats:sup>\u2212<\/jats:sup>\n              in aortas. Tempol, which ablated ONOO\n              <jats:sup>\u2212<\/jats:sup>\n              by scavenging superoxide anion, reduced the effects of nicotine on SIRT1 and collagen. Mutation of zinc-binding cysteine 395 or 398 in SIRT1 into serine (C395S) or (C398S) abolished SIRT1 activity. Furthermore, ONOO\n              <jats:sup>\u2212<\/jats:sup>\n              dose-dependently inhibited the enzyme and increased zinc release in recombinant SIRT1. Finally, we found SIRT1 inactivation by ONOO\n              <jats:sup>\u2212<\/jats:sup>\n              activated the YAP (Yes-associated protein) resulting in abnormal ECM (extracellular matrix) remodeling.\n            <\/jats:p>\n          <\/jats:sec>\n          <jats:sec>\n            <jats:title>Conclusions\u2014<\/jats:title>\n            <jats:p>\n              Nicotine induces ONOO\n              <jats:sup>\u2212<\/jats:sup>\n              , which selectively inhibits SIRT1 resulting in a YAP-mediated ECM remodeling.\n            <\/jats:p>\n            <jats:sec>\n              <jats:title>Visual Overview\u2014<\/jats:title>\n              <jats:p>An online visual overview is available for this article.<\/jats:p>\n            <\/jats:sec>\n          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Atlanta."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ping","family":"Song","sequence":"additional","affiliation":[{"name":"From the Center for Molecular and Translational Medicine, Georgia State University, Atlanta."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ming-Hui","family":"Zou","sequence":"additional","affiliation":[{"name":"From the Center for Molecular and Translational Medicine, Georgia State University, 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