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Furthermore, mutations in LRRK2 and VPS35 compromise vesicle trafficking and endosomal recycling pathways, disrupting synaptic vesicle turnover [197, 198, 199]

suggest that hyperglycemia-induced oxidative stress affects protease-activated receptor 2-mediated vasodilation in the endothelium through a NOX-triggered signaling cascade, which can be suppressed by SGLT2i (200)

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