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However, whether irisin influences the development of diabetic cardiomyopathy (DCM) remains unclear. Therefore, we investigated the potential role and mechanism of action of irisin in diabetes\u2010induced myocardial dysfunction in mice. Type 1 diabetes was induced in mice by injecting streptozotocin, and the diabetic mice were administered recombinant r\u2010irisin (low or high dose: 0.5 or 1.5\u00a0\u03bcg\/g body weight\/day, I.P.) or PBS for 16\u00a0weeks. Irisin treatment did not alter blood glucose levels in the diabetic mice. However, the results of echocardiographical and histopathological assays indicated that low\u2010dose irisin treatment alleviated cardiac fibrosis and left ventricular function in the diabetic mice, whereas high\u2010dose irisin failed to mitigate the ventricular function impairment and increased collagen deposition. The potential mechanism underlying the effect of low\u2010dose irisin involved irisin\u2010mediated inhibition of high glucose\u2010induced endothelial\u2010to\u2010mesenchymal transition (EndMT); conversely, high\u2010dose irisin treatment enhanced high glucose\u2010induced MMP expression by stimulating MAPK (p38 and ERK) signalling and cardiac fibroblast proliferation and migration. Low<jats:bold>\u2010<\/jats:bold>dose irisin alleviated DCM development by inhibiting high glucose\u2010induced EndMT. By contrast, high\u2010dose irisin disrupted normal MMP expression and induced cardiac fibroblast proliferation and migration, which results in excess collagen deposition. Thus, irisin can inhibit high glucose\u2010induced EndMT and exert a dose\u2010dependent bidirectional effect on DCM.<\/jats:p>","DOI":"10.1111\/jcmm.13360","type":"journal-article","created":{"date-parts":[[2017,10,24]],"date-time":"2017-10-24T03:28:56Z","timestamp":1508815736000},"page":"808-822","source":"Crossref","is-referenced-by-count":63,"title":["Irisin inhibits high glucose\u2010induced endothelial\u2010to\u2010mesenchymal transition and exerts a dose\u2010dependent bidirectional effect on diabetic cardiomyopathy"],"prefix":"10.1111","volume":"22","author":[{"given":"Xue","family":"Liu","sequence":"first","affiliation":[{"name":"The Key Laboratory of Cardiovascular Remodeling and Function Research Chinese Ministry of Education and Chinese Ministry of Public Health Qilu Hospital of Shandong University Jinan Shandong China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Haroon","family":"Mujahid","sequence":"additional","affiliation":[{"name":"The Key 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