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. 2022 Aug 15;13:958790. doi: 10.3389/fimmu.2022.958790

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Copyright © 2022 Chen, Liu, He and Li

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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Overview of the pathogenesis of DN. In the diabetic milieu, hyperglycemia, advanced glycation end-products (AGEs), angiotensin II, and oxidative stress activate a variety of signaling cascades driving the recruitment and activation of immune cells to promote the development of inflammation and ultimately leading to a series of pathological changes in DN. AGEs, advanced glycation end products; DAMPs, damage associated molecular patterns; PRRs, pattern recognition receptors; GBM, glomerular basement membrane.