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. 2022 Nov 1;9:973856. doi: 10.3389/fmed.2022.973856

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Copyright © 2022 Casciano, Zauli, Rimondi, Mura, Previati, Busin and Zauli.

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(s) 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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Schematic representation of the effects of the mTOR pathway in diabetic retinopathy (DR). Hyperglycemia and hypoxia prompt a plethora of effects associated with the expression of the PI3K/Akt/mTOR pathway, reactive oxygen species (ROS), advanced glycation end products (AGEs), inflammatory cytokines, and glycolysis intermediates, which in turn sustain vascular leakage and overall inflammation of the retina, with the loss of the blood–retina barrier and the neural microenvironment being mainly driven by increased vascular endothelial growth factor (VEGF) production and dysregulated autophagy.