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Recent evidence suggests excessive mechanical stress (eMS) as an essential role in the pathogenesis of OA. Increased levels of integrin \u03b1V\u03b23 have been detected in osteoarthritic cartilage and were previously implicated in OA pathogenesis. However, the role of integrin \u03b1V\u03b23 in the process of eMS-induced OA remains unclear. Here, histologic and proteomic analyses of osteoarthritic cartilage in a rat destabilization of the medial meniscus model demonstrated elevated expression of integrin \u03b1V\u03b23 as well as more serious cartilage degeneration in the medial weight-bearing area. Furthermore, results of <jats:italic>in vitro<\/jats:italic> study demonstrated that eMS led to a significant increase of integrin \u03b1V\u03b23 expression and phosphorylation of downstream signaling molecules such as FAK and ERK, as well as upregulated expressions of inflammatory and degradative mediators. In addition, we found that inhibition of integrin \u03b1V\u03b23 could alleviate chondrocyte inflammation triggered by eMS both <jats:italic>in vivo<\/jats:italic> and <jats:italic>in vitro<\/jats:italic>. Our findings suggest a central role for upregulation of integrin \u03b1V\u03b23 signaling in OA pathogenesis and demonstrate that activation of integrin \u03b1V\u03b23 signaling in cartilage contributes to inflammation and joint destruction in eMS-induced OA. Taken together, our data presented here provide a possibility for targeting integrin \u03b1V\u03b23 signaling pathway as a disease-modifying therapy.<\/jats:p>","DOI":"10.1007\/s10753-022-01770-6","type":"journal-article","created":{"date-parts":[[2022,12,8]],"date-time":"2022-12-08T16:10:58Z","timestamp":1670515858000},"page":"739-751","update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":22,"title":["Integrin \u03b1V\u03b23 Signaling in the Progression of Osteoarthritis Induced by Excessive Mechanical Stress"],"prefix":"10.1007","volume":"46","author":[{"given":"Fanglong","family":"Song","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Xiaoyu","family":"Mao","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jun","family":"Dai","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Bingchen","family":"Shan","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Zhentao","family":"Zhou","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yifan","family":"Kang","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"297","published-online":{"date-parts":[[2022,12,8]]},"reference":[{"key":"1770_CR1","doi-asserted-by":"crossref","unstructured":"Felson, D. 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