{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,30]],"date-time":"2026-09-30T05:13:09Z","timestamp":1790745189122,"version":"4.1.0"},"reference-count":45,"publisher":"Oxford University Press (OUP)","issue":"8","license":[{"start":{"date-parts":[[2016,10,1]],"date-time":"2016-10-01T00:00:00Z","timestamp":1475280000000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/academic.oup.com\/pages\/standard-publication-reuse-rights"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2016,10,15]]},"abstract":"<jats:title>Abstract<\/jats:title>\n               <jats:p>Systemic sclerosis (SSc) is an autoimmune disease characterized by fibrosis of the skin and visceral organs and vascular alterations. SSc pathophysiology involves systemic inflammation and oxidative stress. Because the vanin-1 gene (vnn1) encodes an enzyme with pantetheinase activity that converts vasculoprotective pantethine into profibrotic pantothenic acid and pro-oxidant cystamine, we tested this pathway in the pathophysiology of SSc. Activation of the vanin-1\/pantetheinase pathway was investigated in wild-type BALB\/c mice with hypochlorous acid (HOCl)-induced SSc by ELISA and Western blotting. We then evaluated the effects of the inactivation of vnn1 on the development of fibrosis, endothelial alterations, and immunological activation in mice with HOCl- and bleomycin-induced SSc. We then explored the vanin-1\/pantetheinase pathway in a cohort of patients with SSc and in controls. In wild-type mice with HOCl-induced SSc, the vanin-1\/pantetheinase pathway was dysregulated, with elevation of vanin-1 activity in skin and high levels of serum pantothenic acid. Inactivation of the vnn1 gene in vnn1\u2212\/\u2212 mice with HOCl-induced SSc prevented the development of characteristic features of the disease, including fibrosis, immunologic abnormalities, and endothelial dysfunction. Remarkably, patients with diffuse SSc also had increased expression of vanin-1 in skin and blood and elevated levels of serum pantothenic acid that correlated with the severity of the disease. Our data demonstrate that vanin-1\/pantetheinase controls fibrosis, vasculopathy, autoimmunity, and oxidative stress in SSc. The levels of vanin-1 expression and pantothenic acid determine SSc severity and can be used as markers of disease severity. More importantly, inhibition of vanin-1 can open new therapeutic approaches in SSc.<\/jats:p>","DOI":"10.4049\/jimmunol.1502511","type":"journal-article","created":{"date-parts":[[2016,9,20]],"date-time":"2016-09-20T01:29:46Z","timestamp":1474334986000},"page":"3326-3335","source":"Crossref","is-referenced-by-count":35,"title":["Imbalance of the Vanin-1 Pathway in Systemic Sclerosis"],"prefix":"10.1093","volume":"197","author":[{"given":"Niloufar","family":"Kavian","sequence":"first","affiliation":[{"name":"Universit\u00e9 Paris Descartes, Sorbonne Paris-Cit\u00e9, Facult\u00e9 de M\u00e9decine, Institut Cochin INSERM U1016 et Laboratoire d\u2019Immunologie Biologique, Assistance Publique H\u00f4pitaux de Paris H\u00f4pital Cochin , 75679 Paris Cedex 14,","place":["France"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Souad","family":"Mehlal","sequence":"additional","affiliation":[{"name":"Universit\u00e9 Paris Descartes, Sorbonne Paris-Cit\u00e9, Facult\u00e9 de 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