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. 2018 Sep 7;42(6):3278–3290. doi: 10.3892/ijmm.2018.3866

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Copyright: © Huang 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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Schematic of the present study, including a description of the mechanism. Under normal circumstances, SNAP29 combines with SXT17 and VAMP8, forming a complex that is involved in the process of autophagosome and lysosome formation. In STZ-induced type I DM, the increase in O-GlcNAc-modified SNAP29 inhibits the formation of the SNAP29-STX17-VAMP8 complex, subsequently affecting autophagosome and lysosomal membrane fusion, which triggers myocardial injury in type I DM. O-GlcNAc, O-linked β-N-acetylglucosamine; SNAP29, synaptosomal-associated protein 29; vesicle-associated membrane protein 8; STX17, syntaxin-17; LC3, microtubule-associated protein 1 light chain 3α; DM, diabetes mellitus.