{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,6,12]],"date-time":"2026-06-12T07:33:43Z","timestamp":1781249623911,"version":"3.54.1"},"reference-count":49,"publisher":"SAGE Publications","issue":"15","license":[{"start":{"date-parts":[[2016,5,1]],"date-time":"2016-05-01T00:00:00Z","timestamp":1462060800000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/journals.sagepub.com\/page\/policies\/text-and-data-mining-license"}],"content-domain":{"domain":["journals.sagepub.com"],"crossmark-restriction":true},"short-container-title":["Antioxidants &amp; Redox Signaling"],"published-print":{"date-parts":[[2016,5]]},"abstract":"<jats:p>\n                    <jats:bold>\n                      <jats:italic toggle=\"yes\">Aims:<\/jats:italic>\n                    <\/jats:bold>\n                    Recent studies have revealed that autophagy is induced under various disease conditions; however, the role of autophagy in pathological states is controversial. NAD(P)H:quinone oxidoreductase 1 (\n                    <jats:italic toggle=\"yes\">NQO1<\/jats:italic>\n                    ) is a highly inducible cytoprotective gene that regulates reactive oxygen species (ROS) generation. In this study, we examined whether\n                    <jats:italic toggle=\"yes\">NQO1<\/jats:italic>\n                    deficiency affects the autophagy process in response to cisplatin-induced nephrotoxicity.\n                    <jats:bold>\n                      <jats:italic toggle=\"yes\">Results:<\/jats:italic>\n                    <\/jats:bold>\n                    <jats:italic toggle=\"yes\">In vitro<\/jats:italic>\n                    ,\n                    <jats:italic toggle=\"yes\">NQO1<\/jats:italic>\n                    and autophagy-associated proteins were induced after cisplatin treatment and the autophagosomes markedly increased in the cisplatin-treated\n                    <jats:italic toggle=\"yes\">NQO1<\/jats:italic>\n                    -knockdown ACHN cells together with increased ROS production.\n                    <jats:italic toggle=\"yes\">In vivo<\/jats:italic>\n                    ,\n                    <jats:italic toggle=\"yes\">NQO1<\/jats:italic>\n                    -KO mice displayed a significant increase in cisplatin-induced acute kidney injury (AKI), as indicated by elevated tubular damage and apoptosis as well as by suppressed cytoprotective signals. In agreement with the\n                    <jats:italic toggle=\"yes\">in vitro<\/jats:italic>\n                    findings,\n                    <jats:italic toggle=\"yes\">NQO1<\/jats:italic>\n                    -KO cisplatin-treated mice displayed a notable increase in autophagy-associated protein expression compared with their wild-type counterparts. Meanwhile, the expression of Ras-related protein 7, which participates in autophagosome maturation and lysosome fusion, markedly decreased in\n                    <jats:italic toggle=\"yes\">NQO1<\/jats:italic>\n                    -KO mice, indicating hampered progress in late autophagy, and was accompanied by increased p62 protein expression. Moreover,\n                    <jats:italic toggle=\"yes\">NQO1<\/jats:italic>\n                    deletion enhanced the effect of the mammalian target of the rapamycin inhibitor, rapamycin, and led to enhanced tuberous sclerosis complex 2 phosphorylation through AMP-activated protein kinase activation.\n                    <jats:bold>\n                      <jats:italic toggle=\"yes\">Innovation and Conclusion:<\/jats:italic>\n                    <\/jats:bold>\n                    These results indicate that autophagy may be enhanced to counter the increased stress due to\n                    <jats:italic toggle=\"yes\">NQO1<\/jats:italic>\n                    deficiency, an oxidative stress barrier. The present results demonstrate the significant influence of\n                    <jats:italic toggle=\"yes\">NQO1<\/jats:italic>\n                    on the autophagy process and support the hypothesis that autophagy plays a protective role under oxidative stress conditions.\n                    <jats:italic toggle=\"yes\">Antioxid. Redox Signal.<\/jats:italic>\n                    24, 867\u2013883.\n                  <\/jats:p>","DOI":"10.1089\/ars.2015.6386","type":"journal-article","created":{"date-parts":[[2016,3,3]],"date-time":"2016-03-03T03:04:17Z","timestamp":1456974257000},"page":"867-883","update-policy":"https:\/\/doi.org\/10.1177\/sage-journals-update-policy","source":"Crossref","is-referenced-by-count":40,"title":["<i>NQO1<\/i>\n                    Deficiency Leads Enhanced Autophagy in Cisplatin-Induced Acute Kidney Injury Through the AMPK\/TSC2\/mTOR Signaling Pathway"],"prefix":"10.1177","volume":"24","author":[{"given":"Tae-Won","family":"Kim","sequence":"first","affiliation":[{"name":"Chungnam National University"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Young-Jung","family":"Kim","sequence":"additional","affiliation":[{"name":"Chungnam National 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