{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,5]],"date-time":"2026-10-05T14:58:04Z","timestamp":1791212284327,"version":"4.1.0"},"reference-count":44,"publisher":"Wiley","issue":"1","license":[{"start":{"date-parts":[[2012,11,16]],"date-time":"2012-11-16T00:00:00Z","timestamp":1353024000000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Aging Cell"],"published-print":{"date-parts":[[2013,2]]},"abstract":"<jats:title>Summary<\/jats:title><jats:p>Aging is accelerated, at least in part, by pathological condition such as metabolic syndrome (MetS), and various molecular pathways such as oxidative stress are common mediators of aging and MetS. We previously developed the aging\u2010like skin model by single ultraviolet (<jats:styled-content style=\"fixed-case\">UV<\/jats:styled-content>) irradiation on the MetS model mice. Recent studies revealed that mineralocorticoid receptor (<jats:styled-content style=\"fixed-case\">MR<\/jats:styled-content>) signaling plays a pivotal role for various tissue inflammation and damages in MetS. Although previous studies reported that <jats:styled-content style=\"fixed-case\">MR<\/jats:styled-content> is expressed in the skin and that overexpression of <jats:italic><jats:styled-content style=\"fixed-case\">MR<\/jats:styled-content><\/jats:italic> in the skin resulted in the skin atrophy, the physiological or pathological functions of <jats:styled-content style=\"fixed-case\">MR<\/jats:styled-content> in the skin are not fully elucidated. Here, we show the involvement of <jats:styled-content style=\"fixed-case\">MR<\/jats:styled-content> signaling in the aging\u2010like skin changes in our own model. Elevations of oxidative stress and inflammation markers were observed in the MetS mice, and the <jats:styled-content style=\"fixed-case\">UV<\/jats:styled-content>\u2010evoked aging\u2010like skin damages were attenuated by topical antioxidant. <jats:styled-content style=\"fixed-case\">MR<\/jats:styled-content> expression was higher in the MetS mouse skin, and notably, expression of its effecter gene <jats:italic>Sgk1<\/jats:italic> was significantly upregulated in the aging\u2010like skin in the <jats:styled-content style=\"fixed-case\">UV<\/jats:styled-content>\u2010irradiated MetS mice. Furthermore, topical application of <jats:styled-content style=\"fixed-case\">MR<\/jats:styled-content> antagonist spironolactone suppressed <jats:italic>Sgk1<\/jats:italic> expression, oxidative stress, inflammation, and the aging\u2010like changes in the skin. The 2\u2010week <jats:styled-content style=\"fixed-case\">UV<\/jats:styled-content> onto the non\u2010MetS mice, the more usual photoaging model, resulted in the skin damages mostly equivalent to the MetS mice with single <jats:styled-content style=\"fixed-case\">UV<\/jats:styled-content>, but they were not associated with upregulation of <jats:styled-content style=\"fixed-case\">MR<\/jats:styled-content> signaling. Our studies suggested an unexpected role of <jats:styled-content style=\"fixed-case\">MR<\/jats:styled-content> signaling in the skin aging in MetS status.<\/jats:p>","DOI":"10.1111\/acel.12017","type":"journal-article","created":{"date-parts":[[2012,10,17]],"date-time":"2012-10-17T04:12:10Z","timestamp":1350447130000},"page":"50-57","source":"Crossref","is-referenced-by-count":31,"title":["Aging\u2010like skin changes in metabolic syndrome model mice are mediated by mineralocorticoid receptor signaling"],"prefix":"10.1111","volume":"12","author":[{"given":"Takashi","family":"Nagase","sequence":"first","affiliation":[{"name":"Department of Gerontological Nursing\/Wound Care Management Graduate School of Medicine, The University of Tokyo Tokyo 113\u20100033 Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Tomoko","family":"Akase","sequence":"additional","affiliation":[{"name":"Department of Gerontological Nursing\/Wound Care Management Graduate School of Medicine, 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