ArticleNature communications2025
Optineurin-facilitated axonal mitochondria delivery promotes neuroprotection and axon regeneration.
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Article in Nature communications, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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25citing papers in PubMed
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Who cites it
25 citing papers in PubMed.
- Neurodevelopmental miR-135a-1-3p and miR-135b-3p promote long-distance axon regeneration after injury in the central visual pathway.Molecular therapy. Advances · 2026Article
- TIGRa: An ultra-compact programmable activator enabling multiplexed and efficient gene regulation.Cell stem cell · 2026Article
- Towards a systems-level view of the microtubule cytoskeleton and its functions in physiology and disease.Nature reviews. Molecular cell biology · 2026Review
- Review
- Proactively restore visual function: Directly targeting affected retinal neurons.Neural regeneration research · 2026Article
- Targeting OTUD7A-HINT1 deubiquitination activates mTOR signaling for CNS regeneration.Cell death & disease · 2026Article
- Review
- 3'UTR regulation of axon translation and optic nerve regeneration.Molecular neurodegeneration · 2026Article
- The 5-HT1A receptor antagonist WAY-100635 maleate promotes retinal ganglion cell differentiation and protects the retino-visual circuits.Communications medicine · 2026Article
- Optineurin is a gatekeeper of mitochondrial health and proteostasis in Alzheimer's disease vulnerable neurons.bioRxiv : the preprint server for biology · 2026Article
- Actin depolymerization promotes axon regeneration by restoring axonal mitochondrial transport in mouse models of optic neuropathy.Science translational medicine · 2026Article
- The Axon as a Self-Modifying Computational System: Autonomous Inference, Adaptive Propagation, and AI-Enabled Mechanistic Insight.International journal of molecular sciences · 2026Review
- Cell-intrinsic vulnerability and immune activation cooperate to drive degeneration in a mitochondrial complex I deficiency model of optic neuropathy.Journal of neuroinflammation · 2026Article
- From Regeneration Failure to Functional Restoration: Unlocking the Neuronal-Intrinsic Regenerative Capacity as a Therapeutic Frontier for Optic Neuropathy and Glaucoma.CNS neuroscience & therapeutics · 2026Review
- The endo-lysosomal-lipid axis: bidirectional interactions between membrane trafficking dysfunction and lipid metabolic disorders.Frontiers in cell and developmental biology · 2026Review
- Technological advances in axonal regeneration and structural plasticity: optogenetics, single-cell omics, and tissue clearing.Frontiers in cellular neuroscience · 2026Review
- Research progress on molecular therapy for glaucoma (Review).Molecular medicine reports · 2026Review
- Lycium barbarum glycopeptide confers neuroprotection in chronic ocular hypertensive rats: a study investigating visual function, retinal structure, microcirculation, and pyroptosis.Frontiers in pharmacology · 2026Article
- Optineurin Shapes Basal and LPS-Induced Transcriptomes in BV2 Microglia.International journal of molecular sciences · 2025Article
- OPTN protects retinal ganglion cells and ameliorates neuroinflammation in optic neuropathies.Communications biology · 2025Article
Corrections and comments
- Update of
Authors and funding
24 authors.
Dong Liu *Spencer Center for Vision Research, Department of Ophthalmology, Byers Eye Institute at Stanford University School of Medicine, Palo Alto, CA, USA.ORCID http://orcid.org/0000-0001-8941-0812
Hannah C Webber *Spencer Center for Vision Research, Department of Ophthalmology, Byers Eye Institute at Stanford University School of Medicine, Palo Alto, CA, USA.
Fuyun Bian *Spencer Center for Vision Research, Department of Ophthalmology, Byers Eye Institute at Stanford University School of Medicine, Palo Alto, CA, USA.
Yangfan Xu *Spencer Center for Vision Research, Department of Ophthalmology, Byers Eye Institute at Stanford University School of Medicine, Palo Alto, CA, USA.
Manjari Prakash *Institute of Biotechnology, Czech Academy of Sciences, BIOCEV, Vestec, Prague West, Czechia.
Xue FengSpencer Center for Vision Research, Department of Ophthalmology, Byers Eye Institute at Stanford University School of Medicine, Palo Alto, CA, USA.
Ming YangSpencer Center for Vision Research, Department of Ophthalmology, Byers Eye Institute at Stanford University School of Medicine, Palo Alto, CA, USA.
Hang YangSpencer Center for Vision Research, Department of Ophthalmology, Byers Eye Institute at Stanford University School of Medicine, Palo Alto, CA, USA.
In-Jee YouSpencer Center for Vision Research, Department of Ophthalmology, Byers Eye Institute at Stanford University School of Medicine, Palo Alto, CA, USA.ORCID http://orcid.org/0000-0002-6557-5337
Liang LiSpencer Center for Vision Research, Department of Ophthalmology, Byers Eye Institute at Stanford University School of Medicine, Palo Alto, CA, USA.ORCID http://orcid.org/0000-0002-6292-5995
Liping LiuSpencer Center for Vision Research, Department of Ophthalmology, Byers Eye Institute at Stanford University School of Medicine, Palo Alto, CA, USA.
Pingting LiuSpencer Center for Vision Research, Department of Ophthalmology, Byers Eye Institute at Stanford University School of Medicine, Palo Alto, CA, USA.ORCID http://orcid.org/0000-0003-1601-2818
Haoliang HuangSpencer Center for Vision Research, Department of Ophthalmology, Byers Eye Institute at Stanford University School of Medicine, Palo Alto, CA, USA.
Chien-Yi ChangDepartment of Electrical Engineering, Stanford University, Stanford, CA, USA.
Liang LiuSpencer Center for Vision Research, Department of Ophthalmology, Byers Eye Institute at Stanford University School of Medicine, Palo Alto, CA, USA.
Sahil H ShahSpencer Center for Vision Research, Department of Ophthalmology, Byers Eye Institute at Stanford University School of Medicine, Palo Alto, CA, USA.
Anna La TorreDepartment of Cell Biology and Human Anatomy, University of California, Davis, CA, USA.
Derek S WelsbieViterbi Family Department of Ophthalmology, University of California San Diego, San Diego, CA, USA.
Yang SunSpencer Center for Vision Research, Department of Ophthalmology, Byers Eye Institute at Stanford University School of Medicine, Palo Alto, CA, USA.ORCID http://orcid.org/0000-0001-8735-4765
Xin DuanDepartment of Ophthalmology, University of California San Francisco, San Francisco, CA, USA.ORCID http://orcid.org/0000-0001-5260-8972
Jeffrey Louis GoldbergSpencer Center for Vision Research, Department of Ophthalmology, Byers Eye Institute at Stanford University School of Medicine, Palo Alto, CA, USA.ORCID http://orcid.org/0000-0002-1390-7360
Marcus BraunInstitute of Biotechnology, Czech Academy of Sciences, BIOCEV, Vestec, Prague West, Czechia.ORCID http://orcid.org/0000-0003-2026-2238
Zdenek LanskyInstitute of Biotechnology, Czech Academy of Sciences, BIOCEV, Vestec, Prague West, Czechia. zdenek.lansky@ibt.cas.cz.ORCID http://orcid.org/0000-0001-8474-053X
Yang HuSpencer Center for Vision Research, Department of Ophthalmology, Byers Eye Institute at Stanford University School of Medicine, Palo Alto, CA, USA. huyang@stanford.edu.ORCID http://orcid.org/0000-0002-7980-1649
Funding
Stanford Vision Research CoreP30EY026877 · NEI · STANFORD UNIVERSITY · PI TIRIN MOORE · 2017 to 2026
$8.0MElucidating Neuron-Intrinsic Molecular Mechanisms of Optic Nerve RegenerationR01EY024932 · NEI · TEMPLE UNIV OF THE COMMONWEALTH · PI Yang Hu · 2015 to 2026
$4.8MNeuroprotection by Modulating ER Stress in GlaucomaR01EY023295 · NEI · TEMPLE UNIV OF THE COMMONWEALTH · PI HU, YANG · 2013 to 2022
$3.8MThe role of primary cilia in glaucoma pathogenesisR01EY025295 · NEI · STANFORD UNIVERSITY · PI Yang Sun · 2016 to 2026
$3.5MIn Vivo Function and Metabolism Evaluation of Glaucomatous RGCs by Two-Photon Scanning Laser OphthalmologyR01EY034353 · NEI · STANFORD UNIVERSITY · PI Yang Hu, Hao F Zhang · 2023 to 2026
$2.7MOptineurin dysfunction induces neurodegeneration in normal tension glaucoma by a novel molecular mechanismR01EY032518 · NEI · STANFORD UNIVERSITY · PI Yang Hu · 2022 to 2026
$2.7MPhosphoinositide signaling in glaucoma: rescue strategies for Lowe syndromeR01EY032159 · NEI · STANFORD UNIVERSITY · PI SUN, YANG · 2021 to 2024
$1.6MAnimal Research Equipment, Digital Cages & Metabolic, Avoidance, Fear Conditioning, Place Preference, Self-Administration, Open Field, & Microdialysis Systems for Translational NeuroscienceS10OD030452 · OD · STANFORD UNIVERSITY · PI SHAMLOO, MEHRDAD · 2021 to 2021
$743kLightsheet Microscope for Large-Scale Imaging of Cleared Tissue SamplesS10OD025091 · OD · STANFORD UNIVERSITY · PI DEISSEROTH, KARL A. · 2018 to 2018
$337kElucidation of the Molecular Mechanisms of Optineurin in Glaucomatous DegenerationF32EY029567 · NEI · STANFORD UNIVERSITY · PI WEBBER, HANNAH · 2019 to 2020
$122kNEI NIH HHS F32 EY029567NEI NIH HHS P30 EY026877NEI NIH HHS R01 EY023295NEI NIH HHS R01 EY024932NEI NIH HHS R01 EY025295NEI NIH HHS R01 EY032159NEI NIH HHS R01 EY032518NEI NIH HHS R01 EY034353NIH HHS S10 OD025091NIH HHS S10 OD030452U.S. Department of Health & Human Services | NIH | National Eye Institute (NEI) 1F32EY029567U.S. Department of Health & Human Services | NIH | National Eye Institute (NEI) EY023295U.S. Department of Health & Human Services | NIH | National Eye Institute (NEI) EY024932U.S. Department of Health & Human Services | NIH | National Eye Institute (NEI) EY026877U.S. Department of Health & Human Services | NIH | National Eye Institute (NEI) EY032518U.S. Department of Health & Human Services | NIH | National Eye Institute (NEI) EY034353
Abstract
Optineurin (OPTN) mutations are linked to amyotrophic lateral sclerosis (ALS) and normal tension glaucoma (NTG), but a relevant animal model is lacking, and the molecular mechanisms underlying neurodegeneration are unknown. We find that OPTN C-terminus truncation (OPTN∆C) causes late-onset neurodegeneration of retinal ganglion cells (RGCs), optic nerve (ON), and spinal cord motor neurons, preceded by a decrease of axonal mitochondria in mice. We discover that OPTN directly interacts with both microtubules and the mitochondrial transport complex TRAK1/KIF5B, stabilizing them for proper anterograde axonal mitochondrial transport, in a C-terminus dependent manner. Furthermore, overexpressing OPTN/TRAK1/KIF5B prevents not only OPTN truncation-induced, but also ocular hypertension-induced neurodegeneration, and promotes robust ON regeneration. Therefore, in addition to generating animal models for NTG and ALS, our results establish OPTN as a facilitator of the microtubule-dependent mitochondrial transport necessary for adequate axonal mitochondria delivery, and its loss as the likely molecular mechanism of neurodegeneration.
Indexed as
AxonsMitochondriaNerve RegenerationNeuroprotectionTranscription Factor TFIIIAAmyotrophic Lateral SclerosisAnimalsAxonal TransportCell Cycle ProteinsDisease Models, AnimalHumansLow Tension GlaucomaMaleMembrane Transport ProteinsMiceMice, Inbred C57BLCell Cycle ProteinsMembrane Transport ProteinsOPTN protein, humanOptn protein, mouseTranscription Factor TFIIIA
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LicenceCC BY-NC-ND
Read underepoch 390
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.