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. 2021 Jun 7;9:675486. doi: 10.3389/fcell.2021.675486

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Copyright © 2021 Bao, Qian, Liu, Hong, Che and Wu.

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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A proposed model depicting the p-eIF2α/ATF4/Ihh in regulating hypertrophy and apoptosis of NP cell. TNF-α and BTd promote the phosphorylation of eIF2α and upregulate the ATF4 expression, continuously resulting in the Ihh activation. Suppression of eIF2α phosphorylation by ISRIB decreases the ATF4 and Ihh levels and alleviates the hypertrophy and apoptosis of NP cell. Additionally, CPE treatment suppresses the hypertrophy and apoptosis of NP cell. Thus, disrupting the pathways ultimately protect against the development of IDD. p-eIF2α, phosphorylated eukaryotic initiation factor-2α; ATF4, activating transcription factor 4; Ihh, Indian hedgehog; NP, nucleus pulposus; TNF, tumor necrosis factor; BTd, BTdCPU; eIF2α, eukaryotic initiation factor-2α; CPE, cyclopamine.