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In this study, we investigated the effect of psoriasis\u2010like inflammation (PLI) induced by a cytokine cocktail (interleukin (IL)\u201017A, IL\u201022 and tumour necrosis factor (TNF)\u2010\u03b1) on mitochondrial network morphology and function in cultured keratinocytes (HaCaT) and fibroblasts (BJ\u20105ta). In both cell types, PLI triggered the expression of psoriasis\u2010related Elafin and high amounts of cytokines (IL\u20101, IL\u20106), interferons (IFN\u2010\u03b1, IFN\u2010\u03b2, IFN\u2010\u03b3), and chemokines (C\u2010C motif chemokine 5 (CCL5) and IL\u20108), accompanied by increased mitochondrial membrane potential, reactive oxygen species (ROS) production, respiration suppression, network fragmentation, swelling and cristae disassembly. Stimulated emission depletion (STED) nanoscopy revealed the disappearance of mitochondrial cristae in response to PLI, with the process starting more quickly and being more pronounced in keratinocytes than in fibroblasts. These findings highlight cell\u2010specific mitochondrial responses to psoriatic inflammation, guiding future investigations towards new pharmacological targets for managing psoriasis.<\/jats:p>","DOI":"10.1111\/febs.70301","type":"journal-article","created":{"date-parts":[[2025,10,28]],"date-time":"2025-10-28T15:12:15Z","timestamp":1761664335000},"page":"1191-1211","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":4,"title":["Psoriasis\u2010like inflammation induces structural and functional changes in mitochondria"],"prefix":"10.1111","volume":"293","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-1883-070X","authenticated-orcid":false,"given":"Gabriel\u0117","family":"Kulkovien\u0117","sequence":"first","affiliation":[{"name":"Department of Drug Chemistry, Faculty of Pharmacy Lithuanian University of Health Sciences  Kaunas Lithuania"},{"name":"Laboratory of Pharmaceutical Sciences, Institute of Pharmaceutical Technologies 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