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Current therapeutic development proceeds along several rational axes, including strategies to enhance mitophagy such as USP30 inhibitors (discussed in Section Emerging paradigms: novel mechanisms and druggable targets) and ursodeoxycholic acid, which aim to artificially boost the clearance of damaged mitochondria in patients with residual PINK1-Parkin function [94]

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The KEGG pathway findings demonstrated that transcripts elevated by semaglutide treatment were mainly associated with metabolic pathways involving energy production, amino acid turnover, lipid handling, and xenobiotic metabolism