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. 2018 Jan 15;8:773. doi: 10.1038/s41598-017-19052-9

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© The Author(s) 2018

Open Access This 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 license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license 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 license, visit http://creativecommons.org/licenses/by/4.0/.

PMC Copyright notice

Proposed schematic model of the role of PERK in chondrocyte pathophysiology. When the endoplasmic reticulum (ER) folding capacity controlled by the unfolded protein response is balanced with the demand for extracellular matrix (ECM) secretion, ECM is efficiently secreted, and the health of chondrocytes can be maintained. However, when the demand for ECM secretion exceeds the folding capacity, ECM secretion is decreased, and chondrocytes undergo apoptosis. The translational control mediated by PERK is a critical determinant of this chondrocyte pathophysiology.