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. 2023 Jan 26;14:1120308. doi: 10.3389/fphys.2023.1120308

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Copyright © 2023 Williams, White, Joseph and Hruska.

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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Transcriptional regulation of SOST in the CKD-MBD context: Parathyroid hormone (PTH) inhibits SOST expression through a HDAC5 effect on MEF2 which regulates ECR5. Depending on the cellular context, TGFβ/Activin signaling (via Smad2/3) either up-regulates SOST expression by acting through ECR5 or down-regulates SOST. Hypoxia (via HIF-1α), glucocorticoids and Vitamin D up- or down-regulate SOST expression in a context-dependent manner. TNFα, through a NF-κβ dependent mechanism, and BMP signaling, via Smad1/5/8, increase SOST transcription by targeting the promoter. SOST transcription is negatively regulated by mechanical loading, promoter methylation (DNA-Met) and by epigenetic modifications induced by SIRT1. Zfp467 and transcription factors RUNX2 and SP7 bind to the SOST promoter and activate SOST expression. Adapted from Sebastian and Loots (Bone 96: 76-84, 2018). Graphic created with BioRender.com