Condition focus: Optic Neuropathies & Mitochondrial Dysfunction
Optic neuropathies, including glaucoma, Leber’s hereditary optic neuropathy, dominant optic atrophy, and traumatic optic nerve injury, share mitochondrial dysfunction as a common pathogenic feature despite diverse etiologies. This review examined emerging therapeutic strategies targeting mitochondrial pathways in optic neuropathies, analyzing both genetic and acquired forms to identify shared mechanisms amenable to intervention. The analysis integrated evidence from cellular studies, animal models, and early clinical trials to evaluate mitochondrial-focused therapeutic approaches including metabolic enhancement, antioxidant therapies, and photobiomodulation.
The review established that mitochondrial dysfunction in optic neuropathies manifests through multiple interconnected mechanisms: impaired oxidative phosphorylation leading to ATP depletion in energy-demanding retinal ganglion cells, excessive reactive oxygen species generation causing oxidative damage to mitochondrial DNA and proteins, disrupted mitochondrial dynamics affecting organelle quality control, and triggering of mitochondrial-mediated apoptotic pathways. Therapeutic strategies targeting these pathways showed promise across optic neuropathy subtypes. Photobiomodulation emerged as a particularly attractive approach due to its ability to enhance mitochondrial function through cytochrome c oxidase activation without requiring genetic manipulation or systemic drug administration. The analysis identified critical research priorities including biomarker development for monitoring mitochondrial function in vivo and optimization of treatment timing relative to disease progression.
WaveFront Alignment:
Lopez Sanches’ framework identifying mitochondrial dysfunction as a common therapeutic target across optic neuropathies validates the Spectral WaveFront’s application beyond specific diagnoses, supporting photobiomodulation’s potential to address shared pathogenic mechanisms in diverse optic nerve conditions.
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Editor’s note: Lopez Sanches 2016 establishes mitochondrial therapeutic framework for optic neuropathies. For specific optic nerve photobiomodulation applications, see Rojas 2008, Szymanski 2013, and Fitzgerald 2010. Related mitochondrial targeting review in Gueven 2016. Broader mechanistic context in Beirne 2017.
Related Articles
- Neuroprotective Effects of NIR in Mitochondrial Optic Neuropathy – Rojas 2008
- 670nm Light in Optic Nerve Injury – Szymanski 2013
- NIR Reduces Oxidative Stress in Optic Nerve Injury – Fitzgerald 2010
- Targeting Mitochondrial Function to Treat Optic Neuropathy – Gueven 2016
- Photostimulation of Mitochondria for Retinal Neurodegeneration – Beirne 2017
Key Takeaways
- Mitochondrial dysfunction is common pathogenic feature across diverse optic neuropathies despite different etiologies
- Shared mechanisms include ATP depletion, oxidative stress, disrupted mitochondrial dynamics, and apoptosis triggering
- Photobiomodulation offers mitochondrial enhancement without genetic manipulation or systemic drugs
- Identified critical needs for biomarker development and treatment timing optimization
Study Overview
| Study Type: | Review (therapeutic targets) |
| Wavelength(s): | N/A (therapeutic strategy review) |
| Treatment Protocol: | Analysis of mitochondrial-targeted therapies across optic neuropathy subtypes |
| Sample Size: | Multi-study therapeutic framework synthesis |
| Primary Outcome: | Established mitochondrial dysfunction as common therapeutic target across optic neuropathies |
Full Citation
Lopez Sanches MI, et al. (2016). Emerging mitochondrial therapeutic targets in optic neuropathies. Pharmacol Ther, 165:132-152. View Publication
