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The expression of Col1, Col3 and \u03b1\u2010SMA<\/jats:styled-content> was upregulated in HS<\/jats:styled-content>\u2010derived fibroblasts (HSF<\/jats:styled-content>) exposed to HG<\/jats:styled-content> (20 and 30\u00a0mmol\/L), and HG<\/jats:styled-content> activated the phosphorylated protein expression of IGF<\/jats:styled-content>\/Akt\/mTOR<\/jats:styled-content> signalling pathway in HSF<\/jats:styled-content>. Dpp4, a marker targeted the treatment of diabetes mellitus, was overexpressed in HG<\/jats:styled-content>\u2010induced HSF<\/jats:styled-content>. Linagliptin, a Dpp4 inhibitor, played the antifibrotic role in HSF<\/jats:styled-content> exposed to HG<\/jats:styled-content>, the levels of Col1, Col3 and \u03b1\u2010SMA<\/jats:styled-content> were significantly downregulated, and the cell proliferation and migration were also inhibited. Furthermore, linagliptin alleviated the phosphorylated protein expression of IGF<\/jats:styled-content>\/Akt\/mTOR<\/jats:styled-content> signalling pathway. Moreover, the mTOR<\/jats:styled-content> inhibitor (rapamycin) mimicked the effect of linagliptin on the collagen and \u03b1\u2010SMA<\/jats:styled-content> that means linagliptin may inhibit HG<\/jats:styled-content>\u2010induced transdifferentiation of HSF<\/jats:styled-content> to myofibroblasts via IGF<\/jats:styled-content>\/Akt\/mTOR<\/jats:styled-content> signalling pathway.<\/jats:p>","DOI":"10.1111\/exd.13800","type":"journal-article","created":{"date-parts":[[2018,10,11]],"date-time":"2018-10-11T22:58:17Z","timestamp":1539298697000},"page":"19-27","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":21,"title":["Linagliptin inhibits high glucose\u2010induced transdifferentiation of hypertrophic scar\u2010derived fibroblasts to myofibroblasts via IGF<\/scp>\/Akt\/mTOR<\/scp> signalling pathway"],"prefix":"10.1111","volume":"28","author":[{"given":"Yan","family":"Li","sequence":"first","affiliation":[{"name":"Department of 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