ArticleCell death and differentiation2013
Inhibition of ASK1-p38 pathway prevents neural cell death following optic nerve injury.
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 42 papers.
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Who cites it
42 citing papers in PubMed, 80 citations in OpenAlex.
- Network Analysis of Convergent and Specific Molecular Pathways of Nutraceuticals with Antioxidant and Neuroprotective Potential in Glaucoma.Antioxidants (Basel, Switzerland) · 2026Article
- Preservation of Murine Whole Eyes With Supplemented UW Cold Storage Solution: Anatomical Considerations.Translational vision science & technology · 2024Article
- The cryo-EM structure of ASK1 reveals an asymmetric architecture allosterically modulated by TRX1.eLife · 2024Article
- Inhibition of p38 ameliorates axonal loss with modulation of autophagy in TNF-induced optic nerve damage.International ophthalmology · 2023Article
- ASK1 signaling regulates phase-specific glial interactions during neuroinflammation.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- Strategies for Improving Photodynamic Therapy Through Pharmacological Modulation of the Immediate Early Stress Response.Methods in molecular biology (Clifton, N.J.) · 2022Review
- Apoptosis signal-regulating kinase 1 (ASK1) inhibition reduces endothelial cytokine production without improving permeability after toll-like receptor 4 (TLR4) challenge.Translational research : the journal of laboratory and clinical medicine · 2021Article
- From Oxidative Stress to Inflammation in the Posterior Ocular Diseases: Diagnosis and Treatment.Pharmaceutics · 2021Review
- ASK1/p38‑mediated NLRP3 inflammasome signaling pathway contributes to aberrant retinal angiogenesis in diabetic retinopathy.International journal of molecular medicine · 2021Article
- Non-Cell-Autonomous Regulation of Optic Nerve Regeneration by Amacrine Cells.Frontiers in cellular neuroscience · 2021Review
- Akebia Saponin D prevents axonal loss against TNF-induced optic nerve damage with autophagy modulation.Molecular biology reports · 2020Article
- Suppression of Oxidative Stress as Potential Therapeutic Approach for Normal Tension Glaucoma.Antioxidants (Basel, Switzerland) · 2020Review
- Bioenergetic shift and actin cytoskeleton remodelling as acute vascular adaptive mechanisms to angiotensin II in murine retina and ophthalmic artery.Redox biology · 2020Article
- Nutraceuticals Targeting Generation and Oxidant Activity of Peroxynitrite May Aid Prevention and Control of Parkinson's Disease.International journal of molecular sciences · 2020Review
- DOCK8 is expressed in microglia, and it regulates microglial activity during neurodegeneration in murine disease models.The Journal of biological chemistry · 2019Article
- High hydrostatic pressure induces apoptosis of retinal ganglion cells via regulation of the NGF signalling pathway.Molecular medicine reports · 2019Article
- Recent advances in genetically modified animal models of glaucoma and their roles in drug repositioning.The British journal of ophthalmology · 2019Review
- Differential effects of N-acetylcysteine on retinal degeneration in two mouse models of normal tension glaucoma.Cell death & disease · 2019Article
- Reactive Oxygen Species-Mediated Damage of Retinal Neurons: Drug Development Targets for Therapies of Chronic Neurodegeneration of the Retina.International journal of molecular sciences · 2018Review
- Role of neuritin in retinal ganglion cell death in adult mice following optic nerve injury.Scientific reports · 2018Article
Corrections and comments
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Authors and funding
11 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Optic nerve injury (ONI) induces retinal ganglion cell (RGC) death and optic nerve atrophy that lead to visual loss. Apoptosis signal-regulating kinase 1 (ASK1) is an evolutionarily conserved mitogen-activated protein kinase (MAPK) kinase kinase and has an important role in stress-induced RGC apoptosis. In this study, we found that ONI-induced p38 activation and RGC loss were suppressed in ASK1-deficient mice. Sequential in vivo retinal imaging revealed that post-ONI treatment with a p38 inhibitor into the eyeball was effective for RGC protection. ONI-induced monocyte chemotactic protein-1 production in RGCs and microglial accumulation around RGCs were suppressed in ASK1-deficient mice. In addition, the productions of tumor necrosis factor and inducible nitric oxide synthase in microglia were decreased when the ASK1-p38 pathway was blocked. These results suggest that ASK1 activation in both neural and glial cells is involved in neural cell death, and that pharmacological interruption of ASK1-p38 pathways could be beneficial in the treatment of ONI.
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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.