Nanoengineered mitochondria enable ocular mitochondrial disease therapy via the replacement of dysfunctional mitochondria
Yi Wang, Na-Hui Liu, Li‐Fan Hu, Jingsong Yang, Mengmeng Han, Tian‐Jiao Zhou, Lei Xing, Hu‐Lin Jiang
Abstract
an enhanced PARKIN-mediated mitophagy process. In a mouse model induced with a complex I inhibitor (rotenone, Rot), mNP-Mito enhanced the presence of healthy mitochondria and exhibited a sharp increase in complex I activity (76.5%) compared to the group exposed to Rot damage (29.5%), which greatly promoted the restoration of ATP generation and mitigation of ocular mitochondrial disease-related phenotypes. This study highlights the significance of nanoengineered mitochondria as a promising and feasible tool for the replacement of dysfunctional mitochondria and the repair of mitochondrial function in mitochondrial disease therapies.
Topics & Concepts
MitochondrionDysfunctional familyMitochondrial diseaseMedicineBiologyChemistryBioinformaticsCell biologyMitochondrial DNABiochemistryPsychiatryGeneMitochondrial Function and PathologyPhotoreceptor and optogenetics researchAdvanced Nanomaterials in Catalysis