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. 2021 Jun 10;12:683151. doi: 10.3389/fendo.2021.683151

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Copyright © 2021 Cai, Liu, Men and Zheng

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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Regulation of HN expression under oxidative stress. HN levels in peripheral blood are regulated by IGF and IGFBP. IGFBP-3 is the main component of IGFBP in peripheral blood, with high affinity to HN. IGFBP-3 may transport HN through the blood–brain barrier (Blue dotted arrow), thereby reducing ROS and further protecting nerve cells. Growth hormone down-regulates HN levels in peripheral blood through the high expression of IGF-1. Mitochondrial stressors, such as serum deprivation and chemotherapeutic drugs, increase HN expressions. Anti-apoptotic factors decrease HN expressions. HN levels under oxidative stress may be regulated by increasing IGFBP-3 levels or inhibiting IGF-1 levels.