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Subsequently, we employed\n                      <jats:italic>PIEZO1<\/jats:italic>\n                      knock-out (KO) mice to establish imiquimod (IMQ)-induced psoriasiform models for in vivo experiments. Additionally, we conducted in vitro experiments with\n                      <jats:italic>PIEZO1<\/jats:italic>\n                      -silenced human keratinocytes (HaCaT cells) to investigate the impact on keratinocyte function and the expression of inflammatory cytokines.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      <jats:italic>PIEZO1<\/jats:italic>\n                      expression was significantly upregulated in the basal layer of psoriatic lesions compared to healthy controls. In vivo,\n                      <jats:italic>PIEZO1<\/jats:italic>\n                      KO mice showed attenuated psoriasis-like symptoms, reduced keratinocyte proliferation, inflammatory cell infiltration, and less Th17 cells compared to wild-type mice. Loss of\n                      <jats:italic>PIEZO1<\/jats:italic>\n                      in vitro inhibited keratinocyte proliferation and migration, while inducing apoptosis. Transcriptome sequencing and subsequent analyses revealed that\n                      <jats:italic>PIEZO1<\/jats:italic>\n                      knockdown modulates the NF-kB signaling pathway and associated inflammatory genes. The in vitro activation of NF-kB signaling was diminished by\n                      <jats:italic>PIEZO1<\/jats:italic>\n                      silencing in keratinocytes, resulting in decreased inflammatory cytokine and chemokine expression. Furthermore,\n                      <jats:italic>PIEZO1<\/jats:italic>\n                      facilitated keratinocyte-mediated CD4\u2009+\u2009T cell differentiation into Th17 cells, a key pathogenic factor in psoriasis.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusion<\/jats:title>\n                    <jats:p>\n                      This study highlights the critical role of\n                      <jats:italic>PIEZO1<\/jats:italic>\n                      in psoriatic skin inflammation and suggests that\n                      <jats:italic>PIEZO1<\/jats:italic>\n                      may serve as a novel therapeutic target for psoriasis treatment. Our findings reveal that\n                      <jats:italic>PIEZO1<\/jats:italic>\n                      modulates keratinocyte proliferation, immune cell infiltration, and T cell differentiation through the NF-kB signaling pathway, contributing to the complex pathophysiology of psoriasis.\n                    <\/jats:p>\n                  <\/jats:sec>","DOI":"10.1186\/s10020-025-01279-2","type":"journal-article","created":{"date-parts":[[2025,6,10]],"date-time":"2025-06-10T00:14:01Z","timestamp":1749514441000},"update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":15,"title":["PIEZO1 promotes psoriasis-like skin inflammation in mice via NF-\u03baB\/IL-17 signaling pathway activation"],"prefix":"10.1186","volume":"31","author":[{"given":"Wen","family":"Li","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Kan","family":"Ze","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Xufeng","family":"He","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Lili","family":"Yang","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Huimin","family":"Zhang","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Weian","family":"Yuan","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Wuqing","family":"Wang","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"297","published-online":{"date-parts":[[2025,6,10]]},"reference":[{"key":"1279_CR1","doi-asserted-by":"publisher","unstructured":"Aslani S, Mirarefin SMJ, Zarredar H, Asadi M, Javan MR, Khosrojerdi A, Johnston TP, Sahebkar A. 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