{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,6,1]],"date-time":"2026-06-01T23:21:08Z","timestamp":1780356068326,"version":"3.54.1"},"reference-count":28,"publisher":"Wiley","issue":"11","license":[{"start":{"date-parts":[[2025,6,6]],"date-time":"2025-06-06T00:00:00Z","timestamp":1749168000000},"content-version":"vor","delay-in-days":5,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"funder":[{"DOI":"10.13039\/501100021856","name":"Ministero dell'Universit\u00e0 e della Ricerca","doi-asserted-by":"publisher","award":["NHS \u2010 PNRR\u2010MAD\u20102022\u201012376295"],"award-info":[{"award-number":["NHS \u2010 PNRR\u2010MAD\u20102022\u201012376295"]}],"id":[{"id":"10.13039\/501100021856","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100021856","name":"Ministero dell'Universit\u00e0 e della Ricerca","doi-asserted-by":"publisher","award":["PNRR \u2010 M4C2\u2010I1.3 Project PE_00000019 HEAL ITALIA"],"award-info":[{"award-number":["PNRR \u2010 M4C2\u2010I1.3 Project PE_00000019 HEAL ITALIA"]}],"id":[{"id":"10.13039\/501100021856","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100021856","name":"Ministero dell'Universit\u00e0 e della Ricerca","doi-asserted-by":"publisher","award":["PRIN2022ALJN73"],"award-info":[{"award-number":["PRIN2022ALJN73"]}],"id":[{"id":"10.13039\/501100021856","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100021856","name":"Ministero dell'Universit\u00e0 e della Ricerca","doi-asserted-by":"publisher","award":["PRIN2022XF7XZF"],"award-info":[{"award-number":["PRIN2022XF7XZF"]}],"id":[{"id":"10.13039\/501100021856","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100021856","name":"Ministero dell'Universit\u00e0 e della Ricerca","doi-asserted-by":"publisher","award":["PRINP202243ZAR"],"award-info":[{"award-number":["PRINP202243ZAR"]}],"id":[{"id":"10.13039\/501100021856","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["J Cellular Molecular Medi"],"published-print":{"date-parts":[[2025,6]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n                  <jats:p>\n                    Psoriasis is a systemic immune\u2010mediated disorder involving multiple signalling pathways. Recent attempts to treat psoriasis involve monoclonal antibodies that block different inflammatory pathways. The monoclonal antibody Adalimumab (ADM) is one of the biologics that block the inflammatory cascade of TNF\u2010alpha. We previously demonstrated the involvement of mesenchymal stem cells (MSCs) in psoriasis pathogenesis and showed their responsiveness to ADM, highlighting their dual role as contributors and therapeutic targets. Mitochondrial dysfunction is increasingly recognised in psoriasis, contributing to oxidative stress, altered metabolism, and immune dysregulation. These mitochondrial changes drive chronic inflammation, keratinocyte\u00a0hyperproliferation, and immune activation\u2014hallmarks of psoriasis\u2014making mitochondria a key focus for therapeutic strategies. In this study, we further investigated ADM's impact on mitochondrial morphology and function in MSCs. MSCs were isolated from the skin of psoriatic patients (PSO\u2010MSCs) and healthy controls (C\u2010MSCs), then exposed to H\n                    <jats:sub>2<\/jats:sub>\n                    O\n                    <jats:sub>2<\/jats:sub>\n                    or LPS to mimic the oxidative and inflammatory environment of psoriasis. PSO\u2010MSCs were also treated with ADM for 72\u2009h before mitochondrial analysis. Compared to C\u2010MSCs, PSO\u2010MSCs showed marked mitochondrial abnormalities. ADM treatment partially reversed these alterations, restoring mitochondrial parameters toward control levels under basal conditions. However, ADM failed to prevent mitochondrial dysfunction when additional stress (H\n                    <jats:sub>2<\/jats:sub>\n                    O\n                    <jats:sub>2<\/jats:sub>\n                    or LPS) was introduced. In conclusion, ADM exerts a protective effect on mitochondrial health in MSCs from psoriatic patients, suggesting mitochondria are among its therapeutic targets. Nonetheless, ADM alone cannot counteract further environmental or inflammatory stressors, which may explain symptom relapse observed in clinical settings.\n                  <\/jats:p>","DOI":"10.1111\/jcmm.70642","type":"journal-article","created":{"date-parts":[[2025,6,6]],"date-time":"2025-06-06T10:30:27Z","timestamp":1749205827000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":2,"title":["Effects of Adalimumab on Mitochondria of Psoriatic Mesenchymal Stem Cells"],"prefix":"10.1111","volume":"29","author":[{"given":"Mariangela","family":"Di Vincenzo","sequence":"first","affiliation":[{"name":"Histology\u2010Department of Clinical and Molecular Sciences Universit\u00e0 Politecnica Delle Marche  Ancona Italy"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Anna","family":"Campanati","sequence":"additional","affiliation":[{"name":"Dermatologic Clinic\u2010Department of Clinical and Molecular Sciences 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