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. 2022 Mar 9;20:125. doi: 10.1186/s12951-022-01318-8

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© The Author(s) 2022

Open AccessThis 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 licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence 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 licence, visit http://creativecommons.org/licenses/by/4.0/. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated in a credit line to the data.

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Fig. 12 — Schematic illustrations of the PEG-CZNP induced attenuation of kidney injury from FD. This occurs via the enhancement of the autophagy flux combined with the activation of TFEB, restoration of AKT/mTOR signaling, and antioxidant effects. PEG-CZNPs thereby alleviate inflammatory and fibrosis pathways and attenuate Gb3-mediated kidney injury