ArticleProceedings of the National Academy of Sciences of the United States of America2014
STAT3 promotes survival of mutant photoreceptors in inherited photoreceptor degeneration models.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed, 38 citations in OpenAlex.
- Selective deletion ofiScience · 2026Article
- Time-Resolved Oxidative Stress and Apoptosis in Murine Retina under Acute Hypobaric Hypoxia with Parallel Activation of the LIF-JAK-STAT3 Axis.Molecular neurobiology · 2026Article
- Connecting cilium, stress response, and proteostasis abnormalities inform variant and therapy assessment in RPGRIP1 retinal organoids.Stem cell reports · 2025Article
- Modulation of retinal inflammation delays degeneration in a mouse model of geographic atrophy.Scientific reports · 2025Article
- Understanding TAK1 deficiency in microglia: Dual mechanisms for photoreceptor protection in a mouse model of retinitis pigmentosa.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Leukemia Inhibitory Factor Protects against Degeneration of Cone Photoreceptors Caused by RPE65 Deficiency.Current medicinal chemistry · 2024Article
- Distinct mouse models of Stargardt disease display differences in pharmacological targeting of ceramides and inflammatory responses.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- Modeling inducible neuropathologies of the retina with differential phenotypes in organoids.Frontiers in cellular neuroscience · 2023Article
- Ciliary neurotrophic factor-mediated neuroprotection involves enhanced glycolysis and anabolism in degenerating mouse retinas.Nature communications · 2022Article
- GADD34 Ablation Exacerbates Retinal Degeneration in P23H RHO Mice.International journal of molecular sciences · 2022Article
- miR-181a/b downregulation: a mutation-independent therapeutic approach for inherited retinal diseases.EMBO molecular medicine · 2022Article
- Role of the JAK/STAT pathway in a streptozotocin-induced diabetic retinopathy mouse model.Graefe's archive for clinical and experimental ophthalmology = Albrecht von Graefes Archiv fur klinische und experimentelle Ophthalmologie · 2022Article
- The potential roles of JAK/STAT signaling in the progression of osteoarthritis.Frontiers in endocrinology · 2022Review
- Luteolin delays photoreceptor degeneration in a mouse model of retinitis pigmentosa.Neural regeneration research · 2021Article
- Retinal Proteomics of a Mouse Model of Dystroglycanopathies Reveals Molecular Alterations in Photoreceptors.Journal of proteome research · 2021Article
- STAT3 deficiency in B cells exacerbates uveitis by promoting expansion of pathogenic lymphocytes and suppressing regulatory B cells (Bregs) and Tregs.Scientific reports · 2020Article
- Reprogramming Müller Glia to Regenerate Retinal Neurons.Annual review of vision science · 2020Review
- Mutation-Independent Therapies for Retinal Diseases: Focus on Gene-Based Approaches.Frontiers in neuroscience · 2020Review
- Disrupted Blood-Retina Lysophosphatidylcholine Transport Impairs Photoreceptor Health But Not Visual Signal Transduction.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2019Article
- The coming-of-age of nucleocytoplasmic transport in motor neuron disease and neurodegeneration.Cellular and molecular life sciences : CMLS · 2019Review
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Authors and funding
9 authors at 3 institutions in 2 countries.
Funding
Abstract
Inherited photoreceptor degenerations (IPDs), a group of incurable progressive blinding diseases, are caused by mutations in more than 200 genes, but little is known about the molecular pathogenesis of photoreceptor (PR) death. Increased retinal expression of STAT3 has been observed in response to many retinal insults, including IPDs, but the role of this increase in PR death is unknown. Here, we show that the expression of Stat3 is increased in PRs of the Tg(RHO P347S) and Prph2(rds) (/+) mouse models of IPD and is activated by tyrosine phosphorylation. PR-specific deletion of Stat3 substantially accelerated PR degeneration in both mutant strains. In contrast, increased PR-specific expression of ROSA26 (R26) alleles encoding either WT STAT3 (Stat3(wt)) or the gain-of-function variant STAT3(C) (Stat3(C)) improved PR survival in both models. Moreover, PR signaling in Tg(RHO P347S) mice carrying either a R26-Stat3(wt) or R26-Stat3(C) allele demonstrated increased a-wave amplitude of the scotopic electroretinogram. Phosphorylation of STAT3 at tyrosine 705 was required for the prosurvival effect because an R26-Stat3(Y705F) allele was not protective. The prosurvival role of enhanced Stat3 activity was validated using recombinant adenoassociated virus (rAAV) vector-mediated PR Stat3 expression in Tg(RHO P347S) mice. Our findings (i) establish that the increase in endogenous PR Stat3 expression is a protective response in IPDs, (ii) suggest that therapeutic augmentation of PR Stat3 expression has potential as a common neuroprotective therapy for these disorders, and (iii) indicate that prosurvival molecules whose expression is increased in mutant PRs may have promise as novel therapies for IPDs.
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Registered trials
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.