ArticleNeurobiology of disease2012
JNK2 and JNK3 are major regulators of axonal injury-induced retinal ganglion cell death.
Article in Neurobiology of disease, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 98 papers, 1 of them a synthesis that pooled it.
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Who cites it
98 citing papers in PubMed, 1 synthesis or guideline pooled it, 141 citations in OpenAlex.
- Meta-analysis of transcriptomic changes in optic nerve injury and neurodegenerative models reveals a fundamental response to injury throughout the central nervous system.Molecular vision · 2017Pooled it
- Topical eye treatment with JGRi1, a protein/protein interaction inhibitor, mitigates retinal degeneration.Cell death & disease · 2026Article
- Müller glia derived EVs promote neurite recovery of an enriched population of retinal ganglion like cells derived from hESC retinal organoids after damage.Scientific reports · 2026Article
- Hexarelin promotes the survival of retinal ganglion cells after optic nerve transection.Indian journal of pharmacology · 2026Article
- Aberrant maintenance of developmental transcription factor PAX6 promotes neuronal cell death via JNK3 signaling.Cell death & disease · 2026Article
- IL1A enhances TNF-induced retinal ganglion cell death.Frontiers in aging neuroscience · 2026Article
- MKK4 and MKK7 control degeneration of retinal ganglion cell somas and axons after glaucoma-relevant injury.Cell death discovery · 2025Article
- NLRX1 limits inflammatory neurodegeneration in the anterior visual pathway.Journal of neuroinflammation · 2025Article
- Engineered bio-functional material-based nerve guide conduits for optic nerve regeneration: a view from the cellular perspective, challenges and the future outlook.Regenerative biomaterials · 2025Review
- Downregulation of SARM1 Protects Retinal Ganglion Cell Axonal and Somal Degeneration Via JNK Activation in a Glaucomatous Model of Ocular Hypertension.Investigative ophthalmology & visual science · 2024Article
- Recruitment, regulation, and release: Control of signaling enzyme localization and function by reversible S-acylation.The Journal of biological chemistry · 2024Review
- IOP and glaucoma damage: The essential role of optic nerve head and retinal mechanosensors.Progress in retinal and eye research · 2024Review
- Regulated Cell Death of Retinal Ganglion Cells in Glaucoma: Molecular Insights and Therapeutic Potentials.Cellular and molecular neurobiology · 2023Review
- BAX activation in mouse retinal ganglion cells occurs in two temporally and mechanistically distinct steps.Molecular neurodegeneration · 2023Article
- BAX activation in mouse retinal ganglion cells occurs in two temporally and mechanistically distinct steps.Research square · 2023Article
- c-Jun N-terminal kinase 1 (JNK1) phosphorylates OTX2 transcription factor that regulates early retinal development.Genes & genomics · 2023Article
- HTT (huntingtin) and RAB7 co-migrate retrogradely on a signaling LAMP1-containing late endosome during axonal injury.Autophagy · 2023Article
- Tetrandrine alleviates inflammation and neuron apoptosis in experimental traumatic brain injury by regulating the IRE1α/JNK/CHOP signal pathway.Brain and behavior · 2022Article
- Maprotiline restores ER homeostasis and rescues neurodegeneration via Histamine Receptor H1 inhibition in retinal ganglion cells.Nature communications · 2022Article
- Review
38 more citing papers are in PubMed but not listed here.
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Authors and funding
8 authors at 4 institutions in 1 country.
Funding
Abstract
Glaucoma is a neurodegenerative disease characterized by the apoptotic death of retinal ganglion cells (RGCs). The primary insult to RGCs in glaucoma is thought to occur to their axons as they exit the eye in the optic nerve head. However, pathological signaling pathways that exert central roles in triggering RGC death following axonal injury remain unidentified. It is likely that the first changes to occur following axonal injury are signal relay events that transduce the injury signal from the axon to the cell body. Here we focus on the c-Jun N-terminal kinase (JNK1-3) family, a signaling pathway implicated in axonal injury signaling and neurodegenerative apoptosis, and likely to function as a central node in axonal injury-induced RGC death. We show that JNK signaling is activated immediately after axonal injury in RGC axons at the site of injury. Following its early activation, sustained JNK signaling is observed in axonally-injured RGCs in the form of JUN phosphorylation and upregulation. Using mice lacking specific Jnk isoforms, we show that Jnk2 and Jnk3 are the isoforms activated in injured axons. Combined deficiency of Jnk2 and Jnk3 provides robust long-term protection against axonal injury-induced RGC death and prevents downregulation of the RGC marker, BRN3B, and phosphorylation of JUN. Finally, using Jun deficient mice, we show that JUN-dependent pathways are important for axonal injury-induced RGC death. Together these data demonstrate that JNK signaling is the major early pathway triggering RGC death after axonal injury and may directly link axon injury to transcriptional activity that controls RGC death.
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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 OpenQuestion graph.