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. 2021 Dec 7;4:1366. doi: 10.1038/s42003-021-02896-3

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© The Author(s) 2021

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 1 — The pathogenesis of DN is complex, and the possible mechanisms can be divided into oxidative stress, inflammatory reactions, etc. The possible mechanisms of GV causing CAN, DPN, and cognitive impairment are as follows: a GV increased ROS, which activated the NRLP3 inflammasome and inhibited autonomic ganglion synaptic transmission, thereby leading to CAN; b GV induces oxidative stress and inflammatory response by activating the NF-kB pathway or PKC, thereby causing DPN; c GV causes cognitive impairment by inhibiting Akt/GSK3β pathway to hyperphosphorylate Tau protein. GV glycemic variability, ROS reactive oxygen species, CAN cardiovascular autonomic neuropathy, DPN diabetic peripheral neuropathy.