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. 2012 Sep 15;7(26):2051–2062. doi: 10.3969/j.issn.1673-5374.2012.26.007

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Copyright: © Neural Regeneration Research

This is an open-access article distributed under the terms of the Creative Commons Attribution-Noncommercial-Share Alike 3.0 Unported, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

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Schematic drawing shows PTEN-Akt/mTOR singling pathway in SCI.

PTEN's phosphatase converts phosphatidylinositol (3,4,5)-trisphosphate (PIP₃) into phosphatidylinositol (4,5)-bisphosphate (PIP₂), thus inhibiting downstream Akt and mTOR signaling.

PI3K converts PIP₂ into PIP₃, which can then activate Akt and mTOR, thus enhancing p-S6 expression leading to neuroprotection. Bisperoxovanadium (bpV) and miR-21 may induce Akt/mTOR activation by inhibition of PTEN, finally exert neuroprotective effects.

PTEN: phosphatase and tensin homolog; mTOR: mammalian target of rapamycin; SCI: spinal cord injury; PI3K: phosphoinositide 3-kinases; S6: ribosomal protein S6.