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. 2018 Jun 13;6:125. doi: 10.3389/fped.2018.00125

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Copyright © 2018 Stark, Dammann, Nielsen and Volpe.

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 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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The regulation of inflammation during lung and retina injury in BPD and ROP. The complex interplay of major factors (PAPP-A, IFNγ, IGF-1, IGFBP-3, and NO) in promoting or reducing inflammation and tissue damage is illustrated, and potential targets for therapeutic intervention are identified. IGFBP-3 upregulates NO in both lung microvascular and hematopoietic stem cells (through PI3K-Akt signaling) and promotes IGF-1 activity, thereby decreasing inflammation and endothelial cell death. In addition to nutritional-induced increased IGFBP-3 levels, the interplay of pathways shown here suggests other points for possible direct therapy. For example, direct inhibition of inflammation and IFNγ may inhibit PAPP-A and release IGF-1 production. Targeting IFN may decrease the expression of Ang2, MMP9, IP-9, and IP-10. Abbreviations are as documented in text.