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In this study, we examined the functional role of retinoic acid inducible\u2010gene I (RIG\u2010I),\u00a0a key regulator of epidermal keratinocyte proliferation, in promoting TIMP\u20101 expression. We found that RIG\u2010I\u00a0is overexpressed in keratinocytes of skin injury and underexpressed in skin wound sites of diabetic foot and streptozotocin\u2010induced diabetic mice. Moreover, mice lacking RIG\u2010I developed an aggravated phenotype when subjected to skin injury. Mechanistically, RIG\u2010I promoted keratinocyte proliferation and wound repair by inducing TIMP\u20101 via the NF\u2010\u03baB signaling pathway. Indeed, recombinant TIMP\u20101 directly accelerated HaCaT cell proliferation in vitro and promoted wound healing in <jats:italic>Ddx58<\/jats:italic><jats:sup>\u2212\/\u2212<\/jats:sup> and diabetic mice in vivo. In summary, we demonstrated that RIG\u2010I is a crucial factor that mediates epidermal keratinocyte proliferation and may be a potential biomarker for skin injury severity, thus making it an attractive locally therapeutic target for the treatment of chronic wounds such as diabetic foot.<\/jats:p>","DOI":"10.1002\/jcp.31049","type":"journal-article","created":{"date-parts":[[2023,6,3]],"date-time":"2023-06-03T17:29:41Z","timestamp":1685813381000},"page":"1876-1890","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":8,"title":["RIG\u2010I contributes to keratinocyte proliferation and wound repair by inducing TIMP\u20101 expression through NF\u2010\u03baB signaling pathway"],"prefix":"10.1002","volume":"238","author":[{"given":"Huiyuan","family":"Zhu","sequence":"first","affiliation":[{"name":"Department of Pathology, Shanghai Tenth People's Hospital Tongji University School of Medicine Shanghai 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