{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,2,21]],"date-time":"2026-02-21T00:44:09Z","timestamp":1771634649074,"version":"3.50.1"},"reference-count":31,"publisher":"Wiley","issue":"1","license":[{"start":{"date-parts":[[2017,11,2]],"date-time":"2017-11-02T00:00:00Z","timestamp":1509580800000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Experimental Dermatology"],"published-print":{"date-parts":[[2018,1]]},"abstract":"Abstract<\/jats:title>The process of skin wound healing involves the following three steps: inflammation, tissue formation and tissue remodelling. These optimal steps are required for the development of normal wound healing. Recent reports demonstrated that inflammasomes are involved in the innate immune response. In the present study, we examined whether the activation of inflammasomes affects the process of skin wound repair. The skin wound repair model was established using wild\u2010type (WT<\/jats:styled-content>), NACHT<\/jats:styled-content>, LRR<\/jats:styled-content> and PYD<\/jats:styled-content> domains\u2010containing protein 3 (NALP<\/jats:styled-content>3) knockout (KO<\/jats:styled-content>) and ASC<\/jats:styled-content>\u2010KO<\/jats:styled-content> mice. The wounds were observed every other day, and changes in wound size over time were calculated using photography. Wound repair in NALP<\/jats:styled-content>3\u2010KO<\/jats:styled-content> and ASC<\/jats:styled-content>\u2010KO<\/jats:styled-content> mice was significantly impaired compared with WT<\/jats:styled-content> mice. Isoliquiritigenin, an inhibitor of NALP<\/jats:styled-content>3, decreased the rate of wound repair in WT<\/jats:styled-content> mice. mRNA<\/jats:styled-content> expression of pro\u2010inflammatory cytokines in the wound sites of NALP<\/jats:styled-content>3\u2010KO<\/jats:styled-content> mice was markedly decreased compared with WT<\/jats:styled-content> mice. Treatment with adenosine triphosphate (ATP<\/jats:styled-content>), a ligand of NALP<\/jats:styled-content>3, upregulated the mRNA<\/jats:styled-content> expression of pro\u2010inflammatory cytokines at the wound site and accelerated wound healing in the WT<\/jats:styled-content> mice. Scratch assay revealed that ATP<\/jats:styled-content> accelerated wound closure in mouse embryonic fibroblasts from WT<\/jats:styled-content> mice but not from NALP<\/jats:styled-content>3\u2010KO<\/jats:styled-content> mice. In conclusion, the present study demonstrated that NALP<\/jats:styled-content>3 pathway activation is involved in wound repair, and the topical use of ATP<\/jats:styled-content> may be useful as an effective treatment for accelerating wound healing.<\/jats:p>","DOI":"10.1111\/exd.13441","type":"journal-article","created":{"date-parts":[[2017,9,9]],"date-time":"2017-09-09T02:33:10Z","timestamp":1504924390000},"page":"80-86","source":"Crossref","is-referenced-by-count":54,"title":["Activation of NLRP<\/scp>3 signalling accelerates skin wound healing"],"prefix":"10.1111","volume":"27","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-4836-4001","authenticated-orcid":false,"given":"Hiroyasu","family":"Ito","sequence":"first","affiliation":[{"name":"Department of Informative Clinical Medicine Gifu University Graduate School of Medicine Gifu 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