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. 2020 Jun 8;11(6):439. doi: 10.1038/s41419-020-2620-z

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© The Author(s) 2020

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. 2 — During SCI, the primary injury leads to the production of free radicals and a chronic state of causing ischemia and hypoxia, resulting in glutamate excitotoxicity, lipid peroxidation, calcium influx, edema and cellular damage. Finally, inflammation and immune response affect the integrity of adjacent tissues. Secondary injury leads to demyelination of the axons, glial cell proliferation, the loss of damaged cells and the disconnection of living neurons, culminating in formation of a microenvironment that is not conducive to nerve regeneration.