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However, the underlying mechanism is elusive. Here, we found that CV-A10 infection in mice could suppress Wnt\/\u03b2-catenin signaling by restraining LDL receptor\u2013related protein 6 (LRP6) phosphorylation and \u03b2-catenin accumulation and lead to onychomadesis. Mechanistically, CV-A10 mimics Dickkopf-related protein 1 (DKK1) to interact with Kringle-containing transmembrane protein 1 (KRM1), the CV-A10 cellular receptor. We further found that Wnt agonist (GSK3\u03b2 inhibitor) CHIR99021 can restore nail stem cell differentiation and protect against nail shedding. These findings provide novel insights into the pathogenesis of CV-A10 and related viruses in onychomadesis and guide prognosis assessment and clinical treatment of the disease.<\/jats:p>","DOI":"10.1084\/jem.20231512","type":"journal-article","created":{"date-parts":[[2024,5,9]],"date-time":"2024-05-09T02:21:09Z","timestamp":1715221269000},"update-policy":"https:\/\/doi.org\/10.1084\/jem.crossmarkpolicy","source":"Crossref","is-referenced-by-count":8,"title":["Coxsackievirus A10 impairs nail regeneration and induces onychomadesis by mimicking DKK1 to attenuate Wnt signaling"],"prefix":"10.1084","volume":"221","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-3558-7852","authenticated-orcid":true,"given":"Yingzi","family":"Cui","sequence":"first","affiliation":[{"id":[{"id":"https:\/\/ror.org\/047yhep71","id-type":"ROR","asserted-by":"publisher"}],"name":"CAS Key Laboratory of Pathogen Microbiology and Immunology, Institute of Microbiology, Chinese Academy of Sciences 1 , Beijing, 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