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. 2014 Jun 23;28(8):1291–1303. doi: 10.1210/me.2014-1047

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Copyright © 2014 by the Endocrine Society

This article has been published under the terms of the Creative Commons Attribution License (CC-BY), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Copyright for this article is retained by the author(s). Author(s) grant(s) the Endocrine Society the exclusive right to publish the article and identify itself as the original publisher.

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Figure 7. — A schematic diagram summarizing the results. The diagram shows AR roles in CaOx crystal formation via the AR liver-kidney axis. For the liver part (left-hand side), AR signaling promotes activity of GO in the liver, which increases the biosynthesis of oxalate by converting glyoxylate into oxalate. For the kidney part (right-hand side), AR signaling increases the activity of NADPH oxidase p22-PHOX, which induces the injury to kidney epithelial cells and then further increases CaOx crystals on the damaged cell surface.