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This study sought to assess whether and how FBXL10 can attenuate DCM using a rat streptozotocin (STZ)\u2010induced DCM model system. In the current study, we found that FBXL10 expression was significantly decreased in diabetic rat hearts. FBXL10 protected cells from high glucose (HG)\u2010induced inflammation, oxidative stress, and apoptosis in vitro. In addition, FBXL10 significantly activated PKC \u03b22 signaling pathway in H9c2 cells and rat model. The cardiomyocyte\u2010specific overexpression of FBXL10 at 12 weeks after the initial STZ administration attenuated oxidative stress and inflammation, thereby reducing cardiomyocyte death and preserving cardiac function in these animals. Moreover, FBXL10 protected against DCM via activation of the PKC \u03b22 pathway. In conclusion, FBXL has the therapeutic potential for the treatment of DCM.<\/jats:p>","DOI":"10.1111\/jcmm.14146","type":"journal-article","created":{"date-parts":[[2019,1,31]],"date-time":"2019-01-31T09:47:00Z","timestamp":1548928020000},"page":"2558-2567","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":17,"title":["FBXL10 regulates cardiac dysfunction in diabetic cardiomyopathy via the PKC \u03b22 pathway"],"prefix":"10.1111","volume":"23","author":[{"given":"Leilei","family":"Yin","sequence":"first","affiliation":[{"name":"Department of Cardiology the First Affiliated Hospital of Harbin Medical University  Harbin China"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Yingying","family":"Fang","sequence":"additional","affiliation":[{"name":"Department of Digestive Heilongjiang Institute of traditional Chinese Medicine  Harbin 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