Drug Repurposing Targeting Mitochondrial Dysfunction in Parkinson's Disease: FBXO7-Focused Approach Through Network Analysis and In Silico Molecular Docking

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dc.contributor.authorSamur, Dilara Nemutlu
dc.date.accessioned2026-01-24T12:01:34Z
dc.date.available2026-01-24T12:01:34Z
dc.date.issued2025
dc.departmentAlanya Alaaddin Keykubat Üniversitesi
dc.description.abstractFBXO7 is a promising but underexplored therapeutic target in Parkinson’s disease (PD), having role in mitophagy, proteasomal degradation, and synaptic function. This study aims to investigate the therapeutic potential of targeting mitochondrial dysfunction in PD through an FBXO7-centered drug repurposing approach. A protein-protein interaction (PPI) network was constructed using the STRING database, and Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analyses were performed to identify key pathways associated with FBXO7. Additionally, in silico molecular docking was conducted using the AutoDock Vina algorithm in SwissDock to evaluate the binding affinities of selected clinically approved drugs to FBXO7 and identify promising candidates for potential repurposing in PD treatment. Docking analysis identified several compounds with high binding affinity to FBXO7, including fluorometholone (-6.367 kcal/mol), bendroflumethiazide ( -6.354 kcal/mol), lasofoxifene (-6.173 kcal/mol), penicillin V ( -6.102 kcal/mol), hydromorphone (-6.067 kcal/mol), and cefamandole (-6.036 kcal/mol). These drugs are involved in biological pathways related to mitochondrial function, neuroinflammation, and cellular stress responses, highlighting their potential as disease-modifying agents in PD. However, limitations such as the potential for exacerbating disease progression or systemic side effects may restrict their direct repurposing. This study highlights several clinically approved drugs with high binding affinities to FBXO7, suggesting their potential for targeting mitochondrial dysfunction in PD. While some compounds may present challenges for or direct use, their molecular interactions offer valuable insights for developing novel mitochondrial-targeted therapies. Further experimental validation and structural optimization are required to enhance their therapeutic potential and minimize side effects, paving the way for novel therapeutic strategies in PD.
dc.identifier.doi10.32708/uutfd.1707053
dc.identifier.endpage303
dc.identifier.issn1300-414X
dc.identifier.issn2645-9027
dc.identifier.issue2
dc.identifier.startpage295
dc.identifier.trdizinid1339594
dc.identifier.urihttps://search.trdizin.gov.tr/tr/yayin/detay/1339594
dc.identifier.urihttps://doi.org/10.32708/uutfd.1707053
dc.identifier.urihttps://hdl.handle.net/20.500.12868/4439
dc.identifier.volume51
dc.indekslendigikaynakTR-Dizin
dc.language.isoen
dc.relation.ispartofUludağ Üniversitesi Tıp Fakültesi Dergisi
dc.relation.publicationcategoryMakale - Ulusal Hakemli Dergi - Kurum Öğretim Elemanı
dc.rightsinfo:eu-repo/semantics/openAccess
dc.snmzKA_TR-Dizin_20260121
dc.subjectParkinson's disease
dc.subjectneurodegeneration
dc.subjectdrug repurposing
dc.subjectmitochondrial dysfunction
dc.subjectFBXO7
dc.titleDrug Repurposing Targeting Mitochondrial Dysfunction in Parkinson's Disease: FBXO7-Focused Approach Through Network Analysis and In Silico Molecular Docking
dc.typeArticle

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