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. 2021 Dec 7;8:790513. doi: 10.3389/fmed.2021.790513

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Copyright © 2021 Dusso, Bauerle and Bernal-Mizrachi.

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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Pathogenesis of parathyroid hyperplasia and resistance to calcitriol actions in CKD. Increases in ADAM17 release of TGFα initiate a vicious ADAM17/TGFα-EGFR cycle responsible for elevations in LIP, the dominant negative isoform of C/EBPβ. Reductions in parathyroid C/EBPβ/LIP ratio induce the ADAM17 gene and suppress VDR gene expression exacerbating parathyroid growth and creating resistance to calcitriol actions. Synergistic interactions between 25(OH)D and calcitriol induce C/EBPβ expression to safely counteract both exacerbated growth and VDR reductions.