{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,30]],"date-time":"2026-09-30T23:07:18Z","timestamp":1790809638600,"version":"4.1.0"},"reference-count":45,"publisher":"Wiley","issue":"7","license":[{"start":{"date-parts":[[2013,6,25]],"date-time":"2013-06-25T00:00:00Z","timestamp":1372118400000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by-nc-nd\/3.0\/"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Experimental Dermatology"],"published-print":{"date-parts":[[2013,7]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p>Acne pathogenesis has recently been linked to decreased nuclear FoxO1 levels and increased <jats:styled-content style=\"fixed-case\">mTORC<\/jats:styled-content>1 activity. This hypothesis postulates that antiacne agents either enhance nuclear FoxO activity or inhibit <jats:styled-content style=\"fixed-case\">mTORC<\/jats:styled-content>1. Benzoyl peroxide (BPO), by activation of oxidative stress\u2010inducible kinases, increases nuclear FoxO levels promoting Sestrin3\u2010mediated AMPK activation. Furthermore, BPO\u2010derived ROS may activate AMPK via ataxia\u2013telangiectasia mutated. Isotretinoin and <jats:italic>all\u2010trans<\/jats:italic> retinoic acid may stimulate FoxO gene expression. Doxycycline may enhance FoxOs nuclear retention by inhibiting the expression of exportin 1. Suppression of TNF\u03b1 signalling by tetracyclines, erythromycin and other macrolides may attenuate IKK\u03b2\u2010TSC1\u2010mediated <jats:styled-content style=\"fixed-case\">mTORC<\/jats:styled-content>1 activation. Erythromycin attenuates ERK1\/2 activity and thereby increases TSC2. Azelaic acid may decrease <jats:styled-content style=\"fixed-case\">mTORC<\/jats:styled-content>1 by inhibiting mitochondrial respiration, increasing cellular ROS and nuclear FoxO levels. Antiandrogens may attenuate <jats:styled-content style=\"fixed-case\">mTORC<\/jats:styled-content>1 by suppressing <jats:styled-content style=\"fixed-case\">mTORC<\/jats:styled-content>2\u2010mediated Akt\/TSC2 signalling. This hypothesis unmasks a common mode of action of antiacne agents as either FoxO enhancers or <jats:styled-content style=\"fixed-case\">mTORC<\/jats:styled-content>1 inhibitors and thus provides a rational approach for the development of new antiacne agents.<\/jats:p>","DOI":"10.1111\/exd.12172","type":"journal-article","created":{"date-parts":[[2013,5,15]],"date-time":"2013-05-15T04:58:45Z","timestamp":1368593925000},"page":"502-504","source":"Crossref","is-referenced-by-count":51,"title":["Are therapeutic effects of antiacne agents mediated by activation of <scp>F<\/scp>ox<scp>O<\/scp>1 and inhibition of m<scp>TORC<\/scp>1?"],"prefix":"10.1111","volume":"22","author":[{"given":"Bodo C.","family":"Melnik","sequence":"first","affiliation":[{"name":"Department of Dermatology, Environmental Medicine and Health Theory University of Osnabr\u00fcck Osnabr\u00fcck 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