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. 2019 Sep 10;44(5):1781–1788. doi: 10.3892/ijmm.2019.4335

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Copyright: © Ji et al.

This is an open access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made.

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Cx43 negatively regulated autophagic flux by enhancing mTOR signaling in the glomeruli of a DN rat model. (A) Immunofluorescence results (magnification, x400) indicating the expression of p-mTOR in each group. Blue, nuclear staining (DAPI); green, p-mTOR staining. (B) Western blot analysis of p-mTOR and mTOR. (C) Relative protein level of p-mTOR/mTOR in the control, DN, DN + Cx43 SCR, DN + Cx43 AS groups. The data are presented as the mean ± standard error of the mean, n=3 per group; ^#P<0.05 vs. control group; ^*P<0.05 vs. DN group (Bonferroni's correction). DN, diabetic nephropathy; mTOR, mammalian target of rapamycin.