ArticleInvestigative ophthalmology & visual science2020
Opa1 Deficiency Leads to Diminished Mitochondrial Bioenergetics With Compensatory Increased Mitochondrial Motility.
Article in Investigative ophthalmology & visual science, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 28 citations in OpenAlex.
- Protein Expression Dynamics in Breast Cancer Cells Exposed to Nano-Encapsulated Tarin, the Taro Lectin.Pharmaceutics · 2026Article
- Electron tomography reveals mitochondrial network and cristae remodelling during cell differentiation in the human placenta.Nature communications · 2026Article
- FAM162A Is a Key Regulator of Mitochondrial Structure, Dynamics, and Bioenergetics, Driving Cellular Protection and Longevity.Aging cell · 2026Article
- Uncovering mitochondrial defects in photoreceptors opens therapeutic opportunities for Stargardt disease.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Disrupted energy metabolism is associated with retinal ganglion cell degeneration in autosomal dominant optic atrophy.Science advances · 2026Article
- Tipping the balance: innate and adaptive immunity in mitochondrial disease.Current opinion in immunology · 2025Review
- CRISPRa-Mediated Increase of OPA1 Expression in Dominant Optic Atrophy.International journal of molecular sciences · 2025Article
- Novel in vivo models of autosomal optic atrophy reveal conserved pathological changes in neuronal mitochondrial structure and function.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025Article
- The Balance of MFN2 and OPA1 in Mitochondrial Dynamics, Cellular Homeostasis, and Disease.Biomolecules · 2025Review
- Disruption of mitochondrial homeostasis and permeability transition pore opening in OPA1 iPSC-derived retinal ganglion cells.Acta neuropathologica communications · 2025Article
- Mitochondria in health, disease, and aging.Physiological reviews · 2023Review
- Insights into SGLT2 inhibitor treatment of diabetic cardiomyopathy: focus on the mechanisms.Cardiovascular diabetology · 2023Review
- Article
- Programming axonal mitochondrial maintenance and bioenergetics in neurodegeneration and regeneration.Neuron · 2022Review
- Role of Oxidative Stress in Ocular Diseases Associated with Retinal Ganglion Cells Degeneration.Antioxidants (Basel, Switzerland) · 2021Review
- Trelagliptin ameliorates oxygen-glucose deprivation/reperfusion (OGD/R)-induced mitochondrial dysfunction and metabolic disturbance of endothelial cells.Human cell · 2021Article
- Red Light Irradiation In Vivo Upregulates DJ-1 in the Retinal Ganglion Cell Layer and Protects against Axotomy-Related Dendritic Pruning.International journal of molecular sciences · 2021Article
- Opa1 Deficiency Promotes Development of Retinal Vascular Lesions in Diabetic Retinopathy.International journal of molecular sciences · 2021Article
- Effects of Iron and Zinc on Mitochondria: Potential Mechanisms of Glaucomatous Injury.Frontiers in cell and developmental biology · 2021Review
- The Role of Mitochondria in Optic Atrophy With Autosomal Inheritance.Frontiers in neuroscience · 2021Review
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Purpose: Retinal ganglion cells (RGCs) are susceptible to mitochondrial deficits and also the major cell type affected in patients with mutations in the OPA1 gene in autosomal dominant optic atrophy (ADOA). Here, we characterized mitochondria in RGCs in vitro from a heterozygous B6; C3-Opa1Q285STOP (Opa1+/-) mouse model to investigate mitochondrial changes underlying the pathology in ADOA. Methods: Mouse RGCs were purified from wild-type and Opa1+/- mouse retina by two-step immunopanning. The mitochondria in neurites of RGCs were labeled with MitoTracker Red for structure and motility measurement by time-lapse imaging. Mitochondrial bioenergetics were determined by the real-time measurement of oxygen consumption rate using a Seahorse XFe 96 Extracellular Flux Analyzer. Results: We observed a significant decrease in mitochondrial length in Opa1+/- RGCs with a remarkably higher proportion and density of motile mitochondria along the neurites. We also observed an increased transport velocity with a higher number of contacts between mitochondria in Opa1+/- RGC neurites. The oxygen consumption assays showed a severe impairment in basal respiration, Adenosine triphosphate-linked (ATP-linked) oxygen consumption, as well as reserve respiratory capacity, in RGCs from Opa1+/- mouse retina. Conclusions: Opa1 deficiency leads to significant fragmentation of mitochondrial morphology, activation of mitochondrial motility and impaired respiratory function in RGCs from the B6; C3-Opa1Q285STOP mouse model. This highlights the significant alterations in the intricate interplay between mitochondrial morphology, motility, and energy production in RGCs with Opa1 deficiency long before the onset of clinical symptoms of the pathology.
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