ArticleCell death and differentiation2013
Optic atrophy 1 mediates mitochondria remodeling and dopaminergic neurodegeneration linked to complex I deficiency.
Article in Cell death and differentiation, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers.
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Who cites it
50 citing papers in PubMed, 101 citations in OpenAlex.
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- Disrupted energy metabolism is associated with retinal ganglion cell degeneration in autosomal dominant optic atrophy.Science advances · 2026Article
- The role of mitochondrial dynamics in metabolic dysfunction-associated steatotic liver disease.Frontiers in medicine · 2026Review
- Research Progress on Idebenone in Neurodegenerative Diseases.Aging medicine (Milton (N.S.W)) · 2025Review
- Parkinson's Disease: The Epidemiology, Risk Factors, Molecular Pathogenesis, Prevention, and Therapy.MedComm · 2025Review
- Opantimirs: A class of antagonizing microRNAs that upregulate Opa1 and improve mitochondrial and disuse myopathies.Cell reports. Medicine · 2025Article
- The DRP1 receptor FIS1 is critical to the expansion of triple-negative breast cancer tumor-initiating cells.Cancer cell international · 2025Article
- Optic Atrophy 1: The Conductor of Cellular Harmony and Age-Related Pathologies.Aging and disease · 2025Review
- Molecular Symphony of Mitophagy: Ubiquitin-Specific Protease-30 as a Maestro for Precision Management of Neurodegenerative Diseases.CNS neuroscience & therapeutics · 2025Review
- The integrated stress response promotes neural stem cell survival under conditions of mitochondrial dysfunction in neurodegeneration.Aging cell · 2024Article
- The Role of Rab Proteins in Mitophagy: Insights into Neurodegenerative Diseases.International journal of molecular sciences · 2023Review
- Establishing induced pluripotent stem cell lines from two dominant optic atrophy patients with distinctFrontiers in genetics · 2023Article
- Revealing the Impact of Mitochondrial Fitness During Early Neural Development Using Human Brain Organoids.Frontiers in molecular neuroscience · 2022Review
- Too much death can kill you: inhibiting intrinsic apoptosis to treat disease.The EMBO journal · 2021Review
- Establishment of an in vitro model for analyzing mitochondrial ultrastructure in PRKN-mutated patient iPSC-derived dopaminergic neurons.Molecular brain · 2021Article
- Mfn2 Overexpression Attenuates MPTP Neurotoxicity In Vivo.International journal of molecular sciences · 2021Article
- Differential ROS-Mediated Phosphorylation of Drp1 in Mitochondrial Fragmentation Induced by Distinct Cell Death Conditions in Cerebellar Granule Neurons.Oxidative medicine and cellular longevity · 2021Article
- High-Resolution Respirometry Reveals MPPInternational journal of molecular sciences · 2020Article
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mitochondrial complex I dysfunction has long been associated with Parkinson's disease (PD). Recent evidence suggests that mitochondrial involvement in PD may extend beyond a sole respiratory deficit and also include perturbations in mitochondrial fusion/fission or ultrastructure. Whether and how alterations in mitochondrial dynamics may relate to the known complex I defects in PD is unclear. Optic atrophy 1 (OPA1), a dynamin-related GTPase of the inner mitochondrial membrane, participates in mitochondrial fusion and apoptotic mitochondrial cristae remodeling. Here we show that complex I inhibition by parkinsonian neurotoxins leads to an oxidative-dependent disruption of OPA1 oligomeric complexes that normally keep mitochondrial cristae junctions tight. As a consequence, affected mitochondria exhibit major structural abnormalities, including cristae disintegration, loss of matrix density and swelling. These changes are not accompanied by mitochondrial fission but a mobilization of cytochrome c from cristae to intermembrane space, thereby lowering the threshold for activation of mitochondria-dependent apoptosis by cell death agonists in compromised neurons. All these pathogenic changes, including mitochondrial structural remodeling and dopaminergic neurodegeneration, are abrogated by OPA1 overexpression, both in vitro and in vivo. Our results identify OPA1 as molecular link between complex I deficiency and alterations in mitochondrial dynamics machinery and point to OPA1 as a novel therapeutic target for complex I cytopathies, such as PD.
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