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. 2022 Apr 4;12:42. doi: 10.1186/s13578-022-00776-9

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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. 11 — Overexpression of UBIAD1 elevated antioxidative capacity by preserving Golgi apparatus fragmentation in OGD/R-induced ferroptosis in vitro. A Confocal images showing co-localization of UBIAD1 (red) with Golgi apparatus marker GM130 (green) (Scale bar = 25 μm). B Changes in the Golgi apparatus morphology and ultrastructure in UBIAD1-overexpressing neurons after OGD/R insult as observed by TEM (Scale bar = 500 nm). C Changes in Golgi apparatus morphology and ultrastructure in UBIAD1-siRNA neurons after OGD/R insult as examined under TEM (Scale bar = 500 nm). n = 3, all data are expressed as the mean ± SD, *P < 0.05, **P < 0.01