{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,21]],"date-time":"2026-09-21T21:06:55Z","timestamp":1790024815395,"version":"4.0.1"},"reference-count":49,"publisher":"Oxford University Press (OUP)","license":[{"start":{"date-parts":[[2026,8,10]],"date-time":"2026-08-10T00:00:00Z","timestamp":1786320000000},"content-version":"vor","delay-in-days":221,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"funder":[{"DOI":"10.13039\/501100001809","name":"National Natural Science Foundation of China","doi-asserted-by":"publisher","award":["82572883"],"award-info":[{"award-number":["82572883"]}],"id":[{"id":"10.13039\/501100001809","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100002858","name":"China Postdoctoral Science Foundation","doi-asserted-by":"publisher","award":["2025\u00a0M772347"],"award-info":[{"award-number":["2025\u00a0M772347"]}],"id":[{"id":"10.13039\/501100002858","id-type":"DOI","asserted-by":"publisher"}]},{"name":"Guangdong Provincial Natural Science Foundation of China","award":["2024A1515010485"],"award-info":[{"award-number":["2024A1515010485"]}]},{"name":"Clinical Major Technology Project of the Guangzhou Municipal Health Commission","award":["2026P-ZD025"],"award-info":[{"award-number":["2026P-ZD025"]}]},{"name":"High-level Clinical Research Program of the First Affiliated Hospital of Sun Yat-sen University"},{"name":"Fundamental Research Program of Shanxi Province","award":["202303021212368"],"award-info":[{"award-number":["202303021212368"]}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2026,1,6]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:sec>\n                    <jats:title>Background<\/jats:title>\n                    <jats:p>Keloids, which are characterized by excessive collagen deposition and fibroblast hyperactivation, present significant therapeutic challenges because of their high recurrence rates and incompletely understood pathogenesis. The transforming growth factor-\u03b2 (TGF-\u03b2) pathway is a central driver, but its upstream regulators in the development of skin fibrosis remain elusive. In this study, we aimed to identify novel upstream modulators of skin fibrosis and to elucidate the underlying molecular mechanisms by which these modulators regulate TGF-\u03b2 signaling in keloid pathogenesis.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>We integrated results of transcriptomic and proteomic analyses of patient-derived keloid and normal skin tissues. Functional validation was performed by using primary keloid fibroblasts (KFs) with gain- and loss-of-function approaches, RNA immunoprecipitation sequencing (RIP-seq), and actinomycin D chase assays. Two independent bleomycin-induced skin fibrosis mouse models were employed for in vivo validation.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>Multiomics profiling revealed that caveolae-associated protein 1 (CAVIN1) was consistently downregulated in keloids. CAVIN1 overexpression in KFs suppressed fibrotic phenotypes, including migration, invasion, collagen contraction, and extracellular matrix protein expression. Mechanistically, CAVIN1 directly bound to and stabilized the mitochondrial long noncoding RNA GAS5. This CAVIN1\/GAS5 axis inhibited Drp1\/Fis1-mediated mitochondrial fission and subsequent reactive oxygen species (ROS) production, leading to the attenuation of the canonical TGF-\u03b2\/Smad2\/3 signaling pathway. Critically, GAS5 silencing abrogated the antifibrotic effects of CAVIN1. Furthermore, database screening revealed that the histone deacetylase inhibitor vorinostat was a CAVIN1-upregulating compound. Both AAV-mediated CAVIN1 overexpression and vorinostat treatment significantly ameliorated skin fibrosis in the mouse models.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p>Our study reports a novel CAVIN1\/GAS5 axis that concurrently targets mitochondrial fission and the TGF-\u03b2\/Smad pathway to suppress skin fibrosis. These findings not only reveal a previously unrecognized mechanistic link in keloid pathogenesis but also identify CAVIN1 as a promising therapeutic target, with vorinostat as a potential repurposable drug for treating fibrotic skin disorders.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1093\/burnst\/tkag052","type":"journal-article","created":{"date-parts":[[2026,8,6]],"date-time":"2026-08-06T11:50:32Z","timestamp":1786017032000},"source":"Crossref","is-referenced-by-count":0,"title":["A novel CAVIN1\/GAS5 axis suppresses skin fibrosis through mitochondrial fission-mediated attenuation of the TGF-\u03b2\/Smad pathway"],"prefix":"10.1093","volume":"14","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-5388-5039","authenticated-orcid":false,"given":"Hao","family":"Yang","sequence":"first","affiliation":[{"name":"Department of Burn and Wound Repair, First Affiliated Hospital of Sun Yat-sen University , 58 Zhongshan Er Road, Yuexiu District, Guangzhou 510080 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