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. 2018 Jun 5;11:190. doi: 10.3389/fnmol.2018.00190

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Copyright © 2018 Zhang and Wang.

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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Possible autophagy signaling pathways in traumatic brain injury (TBI). TBI could inhibit phosphatidylinositide 3-kinases (PI3K)/protein kinase B (AKT)/mammalian target of rapamycin (mTOR) pathway and microRNA-27a (miR-27a), activate nuclear factor erythroid 2-related factor 2 (Nrf2), heme oxygenase-1 (HO-1), nicotinamide adenine dinucleotide phosphate, quinine oxidoreductase-1 (NQO-1), forkhead box O 3a (FoxO3a), toll-like receptor 4 (TLR4), nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) and dynamin-related protein 1 (Drp1). Regulation of these molecules by TBI further promotes the formation of autophagosome. This step requires unselective or selective targets, such as damaged mitochondria, for degradation. Mild autophagy leads to adenosine triphosphate (ATP) generation and free amino acid release, which are beneficial for TBI. Conversely, excessive autophagy results in autophagic cell death or apoptosis.