Diagram showing the role of the polo-like kinase 1 (PLK1)-mammalian target of rapamycin (mTOR) axis in sepsis-induced intestinal barrier dysfunction (IMAGE)
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Overexpression of PLK1 enhances intestinal epithelial autophagy during sepsis, thus reducing intestinal epithelial apoptosis and ameliorating intestinal barrier dysfunction. However, the protective effects of PLK1 are impaired by treatment with chloroquine, an inhibitor of autophagy. PLK1 negatively regulates the activity of the mTOR pathway, and the inhibition of mTOR recovers the expression of PLK1, thus generating regulatory crosstalk during sepsis, which may be another mechanism of sepsis-induced intestinal barrier dysfunction. CLP, cecal ligation and puncture; LPS, lipopolysaccharide.
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The American Journal of Pathology
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