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After depolarization of presynaptic neurons, acetylcholine is released into the synaptic cleft and binds to postsynaptic receptors such as acetylcholine muscarinic receptors (mAchRs) or acetylcholine nicotinic receptors (nAchRs) (40)

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On the other hand, DPP-4 inhibitors augment the half-life of endogenous GLP-1 by impeding its degradation

Through HDAC6 inhibition, the pathway promotes the removal of damaged cellular components, reducing oxidative stress and enhancing cellular repair mechanisms in retinal cells ( 2.2.3 Beyond the eye In renal tubular cells ( + -dependent deacetylase SIRT1, reducing mitochondrial dysfunction and oxidative stress by decreasing ROS production, thereby preventing apoptosis induced by lipotoxicity