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Various models of AMPK activation have been established and widely used, including energy deprivation, induction of intracellular calcium, and use of a pharmacological activator to induce phosphorylation of the AMPK subunit at the Thr-172 residue, leading to enhanced epithelial barrier functions and TJ assembly

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The lipid bilayer protects this drug from degradation and thereby enables its accumulation in tumor tissues through the EPR effect

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