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. 2022 Aug 17;11(16):2560. doi: 10.3390/cells11162560

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© 2022 by the authors.

Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/).

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Figure A9 — MaR1 improves the osteogenic effect in type 2 diabetic osteoporosis by activating the NRF pathway and inhibiting high-glucose-induced ferroptosis in osteoblasts. In the condition of diabetes, high glucose levels inhibit the activation and translocation of NRF2 to the nucleus so that the downstream factor SLC7A11/GPX4 does not play its antioxidant role well, and cell membrane lipid peroxidation occurs at high rates, resulting in cell ferroptosis, and the osteogenic effect is significantly reduced. Under conditions of diabetes and supply of MaR1, the NRF pathway is activated, nuclear translocation occurs, the expression of SLC7A11/GPX4 is up-regulated, and lipid peroxidation is inhibited. As a result, cell ferroptosis is inhibited, osteogenic capacity is enhanced, and type 2 diabetic osteoporosis is improved. The figure was partly generated using Servier Medical Art, provided by Servier, licensed under a Creative Commons Attribution 3.0 unported license. NRF2: nuclear factor erythroid-2 related factor 2; SLC7A11: cystine-glutamate antiporter; GSH: glutathione; GPX4: glutathione peroxidase 4; Lipid ROS: lipid reactive oxygen species.