{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,30]],"date-time":"2026-09-30T23:08:18Z","timestamp":1790809698430,"version":"4.1.0"},"reference-count":70,"publisher":"Wiley","issue":"1","license":[{"start":{"date-parts":[[2012,12,27]],"date-time":"2012-12-27T00:00:00Z","timestamp":1356566400000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Experimental Dermatology"],"published-print":{"date-parts":[[2013,1]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p>Azelaic acid (AzA) has been used for the treatment for inflammatory skin diseases, such as acne and rosacea. Interestingly, an improvement in skin texture has been observed after long\u2010time treatment with AzA. We previously unrevealed that anti\u2010inflammatory activity of AzA involves a specific activation of PPAR\u03b3, a nuclear receptor that plays a relevant role in inflammation and even in ageing processes. As rosacea has been considered as a photo\u2010aggravated disease, we investigated the ability of AzA to counteract stress\u2010induced premature cell senescence (SIPS). We employed a SIPS model based on single exposure of human dermal fibroblasts (HDFs) to UVA and 8\u2010methoxypsoralen (PUVA), previously reported to activate a senescence\u2010like phenotype, including long\u2010term growth arrest, flattened morphology and increased synthesis of matrix metalloproteinases (MMPs) and senescence\u2010associated \u03b2\u2010galactosidase (SA\u2010\u03b2\u2010gal). We found that PUVA\u2010treated HDFs grown in the presence of AzA maintained their morphology and reduced MMP\u20101 release and SA\u2010\u03b2\u2010galactosidase\u2010positive cells. Moreover, AzA induced a reduction in ROS generation, an up\u2010modulation of antioxidant enzymes and a decrease in cell membrane lipid damages in PUVA\u2010treated HDFs. Further evidences of AzA anti\u2010senescence effect were repression of p53 and p21, increase in type I pro\u2010collagen and abrogation of the enhanced expression of growth factors, such as HGF and SCF. Interestingly, PUVA\u2010SIPS showed a decreased activation of PPAR\u03b3 and AzA counteracted this effect, suggesting that AzA effect involves PPAR\u03b3 modulation. All together these data showed that AzA interferes with PUVA\u2010induced senescence\u2010like phenotype and its ability to activate PPAR\u2010\u03b3 provides relevant insights into the anti\u2010senescence mechanism.<\/jats:p>","DOI":"10.1111\/exd.12066","type":"journal-article","created":{"date-parts":[[2012,11,23]],"date-time":"2012-11-23T01:55:08Z","timestamp":1353635708000},"page":"41-47","source":"Crossref","is-referenced-by-count":59,"title":["Azelaic acid reduced senescence\u2010like phenotype in photo\u2010irradiated human dermal fibroblasts: possible implication of PPAR\u03b3"],"prefix":"10.1111","volume":"22","author":[{"given":"Stefania","family":"Briganti","sequence":"first","affiliation":[{"name":"Cutaneous Physiopatology Laboratory San Gallicano Dermatology Institute Rome Italy"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Enrica","family":"Flori","sequence":"additional","affiliation":[{"name":"Cutaneous Physiopatology Laboratory San Gallicano 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