Linagliptin inhibits high glucose-induced trans-differentiation of hypertrophic scar derived fibroblasts to myofibroblasts via IGF/Akt/mTOR signali…
Authors of this article are:
Li Y, Zhang J, Zhou Q, Wang H, Xie S, Yang X, Ji P, Zhang W, He T, Liu Y, Wang K, Li X, Shi J, Hu D.
A summary of the article is shown below:
Hypertrophic scar (HS) is a fibro-proliferative disease after serious burns, the underlying mechanism remains unknown. The study was performed to clarify the effect of high glucose (HG) on HS. The expression of Col1, Col3 and α-SMA were up-regulated in HS derived fibroblasts (HSFs) exposed to HG (20mM, 30mM), and HG activated the phosphorylated protein expression of IGF/Akt/mTOR signaling pathway in HSFs. Dpp4, a marker targeted the treatment of diabetes mellitus, was overexpressed in HG-induced HSFs. Linagliptin, a Dpp4 inhibitor, played the anti-fibrosis role in HSFs exposed to HG, the levels of Col1, Col3 and α-SMA were significantly down-regulated, the cell proliferation and migration was also inhibited.. Furthermore, linagliptin alleviated the phosphorylated protein expression of IGF/Akt/mTOR signaling pathway. Moreover, the mTOR inhibitor (rapamycin) mimicked the effect of linagliptin on the collagen and α-SMA, that means linagliptin may inhibit HG-induced trans-differentiation of HSFs to myofibroblasts via IGF/Akt/mTOR signaling pathway. This article is protected by copyright. All rights reserved.
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