ArticleMolecular neurodegeneration2015
Caspase-7: a critical mediator of optic nerve injury-induced retinal ganglion cell death.
Article in Molecular neurodegeneration, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
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Who cites it
32 citing papers in PubMed, 47 citations in OpenAlex.
- Experimental models to study oxidative stress in glaucoma: integratingFrontiers in pharmacology · 2026Review
- The Role of Connexin 36 Gap Junctions in Retinal Ganglion Cell Death After Corneal Alkali Burns.Investigative ophthalmology & visual science · 2025Article
- The molecular mechanisms underlying retinal ganglion cell apoptosis and optic nerve regeneration in glaucoma (Review).International journal of molecular medicine · 2025Review
- RIP1 inhibition protects retinal ganglion cells in glaucoma models of ocular injury.Cell death and differentiation · 2025Article
- Caspase-mediated pathways in retinal ganglion cell injury: a novel therapeutic target for glaucoma.Frontiers in cell and developmental biology · 2025Review
- CCL4 contributes to aging related angiogenic insufficiency through activating oxidative stress and endothelial inflammation.Angiogenesis · 2024Article
- Exploring caspase functions in mouse models.Apoptosis : an international journal on programmed cell death · 2024Review
- Apoptosis in glaucoma: A new direction for the treatment of glaucoma (Review).Molecular medicine reports · 2024Review
- The broad impact of cell death genes on the human disease phenome.Cell death & disease · 2024Article
- Regulated Cell Death of Retinal Ganglion Cells in Glaucoma: Molecular Insights and Therapeutic Potentials.Cellular and molecular neurobiology · 2023Review
- Apoptotic cell death in disease-Current understanding of the NCCD 2023.Cell death and differentiation · 2023Review
- Calpains as mechanistic drivers and therapeutic targets for ocular disease.Trends in molecular medicine · 2022Review
- Effect of retinol and α-tocopherol supplementation on photoreceptor and retinal ganglion cell apoptosis in diabetic rats model.International journal of retina and vitreous · 2022Article
- Early-Onset Glaucoma inBiomedicines · 2022Article
- Retinal ganglion cell loss in an ex vivo mouse model of optic nerve cut is prevented by curcumin treatment.Cell death discovery · 2021Article
- A differential loss of nerve fiber layer thickness and retinal ganglion cell complex in toxic and nutritional optic neuropathy.Advances in ophthalmology practice and research · 2021Article
- Whole-Genome Methylation Analysis Revealed ART-Specific DNA Methylation Pattern of Neuro- and Immune-System Pathways in Chinese Human Neonates.Frontiers in genetics · 2021Article
- Integrin CD11b Deficiency Aggravates Retinal Microglial Activation and RGCs Degeneration After Acute Optic Nerve Injury.Neurochemical research · 2020Article
- Inducible rodent models of glaucoma.Progress in retinal and eye research · 2020Review
- Prospective Application of Activity-Based Proteomic Profiling in Vision Research-Potential Unique Insights into Ocular Protease Biology and Pathology.International journal of molecular sciences · 2019Review
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundAxonal injury of the optic nerve (ON) is involved in various ocular diseases, such as glaucoma and traumatic optic neuropathy, which leads to apoptotic death of retinal ganglion cells (RGCs) and loss of vision. Caspases have been implicated in RGC pathogenesis. However, the role of caspase-7, a functionally unique caspase, in ON injury and RGC apoptosis has not been reported previously. The purpose of this study is to evaluate the role of caspase-7 in ON injury-induced RGC apoptosis.
resultsC57BL/6 (wildtype, WT) and caspase-7 knockout (Casp7(-/-)) mice were used. We show that ON crush activated caspase-7 and calpain-1, an upstream activator of caspase-7, in mouse RGCs, as well as hydrolysis of kinectin and co-chaperone P23, specific substrates of caspase-7. ON crush caused a progressive loss of RGCs to 28 days after injury. Knockout of caspase-7 partially and significantly protected against the ON injury-induced RGC loss; RGC density at 28 days post ON crush in Casp7(-/-) mice was approximately twice of that in WT ON injured retinas. Consistent with changes in RGC counts, spectral-domain optical coherence tomography analysis revealed that ON crush significantly reduced the in vivo thickness of the ganglion cell complex layer (including ganglion cell layer, nerve fiber layer, and inner plexiform layer) in the retina. The ON crush-induced thinning of retinal layer was significantly ameliorated in Casp7(-/-) mice when compared to WT mice. Moreover, electroretinography analysis demonstrated a decline in the positive component of scotopic threshold response amplitude in ON crushed eyes of the WT mice, whereas this RGC functional response was significantly higher in Casp7(-/-) mice at 28 days post injury.
conclusionAltogether, our findings indicate that caspase-7 plays a critical role in ON injury-induced RGC death, and inhibition of caspase-7 activity may be a novel therapeutic strategy for glaucoma and other neurodegenerative diseases of the retina.
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