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Mutations in parkin ( PRKN ) or phosphate and tensin homolog-induced kinase 1 ( PINK1 ) prevent cells from responding to mitochondrial damage by altering the balance of fusion to fission and disrupting mitophagy, which leads to familial forms of PD [97, 98]

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Surface functionalization and structural engineering are therefore essential to enhance stability, biocompatibility, and multifunctionality for biomedical applications