Like MPP+, PD-associated mutations (e.g., in PINK1, Parkin) disrupt complex I–driven OXPHOS [67, 68], but our work reveals VEGF’s ability to restore coupling efficiency even after MPP+ damage, a mechanism distinct from prior studies focusing on VEGF’s angiogenic or anti-apoptotic roles [10, 55]. This evidence concerns the gene PRKN and Parkinson disease.