ArticleThe Journal of clinical investigation2015
Activated mTORC1 promotes long-term cone survival in retinitis pigmentosa mice.
Article in The Journal of clinical investigation, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 108 papers.
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Who cites it
108 citing papers in PubMed, 169 citations in OpenAlex.
- Metabolomics Effects of Folding Correction in Retinitis Pigmentosa Rhodopsin Mutant P23A.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026Article
- N-acetylcysteine suppresses retinal defects in Drosophila models of SNRNP200-associated retinitis pigmentosa.Human molecular genetics · 2026Article
- An siRNA targetingMolecular therapy. Nucleic acids · 2026Article
- Mitochondrial Dysfunction and Oxidative Stress in Retinal Degeneration: Mechanisms, Biomarkers, and Therapeutic Perspectives.Current issues in molecular biology · 2026Review
- Elevating Jak-STAT signaling via SOCS3 deletion sustains photoreceptor viability and visual function in mouse models of retinitis pigmentosa.Cell communication and signaling : CCS · 2026Article
- Selective deletion ofiScience · 2026Article
- Nutrient supplementation mitigates retinal dysfunction in Acox1 knockout mice with impaired peroxisomal fatty acid oxidation.Journal of advanced research · 2025Article
- Age-Related Macular Degeneration: Cellular and Molecular Signaling Mechanisms.International journal of molecular sciences · 2025Review
- Role of alpha-1 antitrypsin in Bruch's membrane integrity.Scientific reports · 2025Article
- RPE-specific MCT2 expression promotes cone survival in models of retinitis pigmentosa.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- A review of the 661W cell line as a tool to facilitate treatment development for retinal diseases.Cell & bioscience · 2025Review
- Pten Loss Triggers Progressive Photoreceptor Degeneration in an mTORC1-Independent Manner.Investigative ophthalmology & visual science · 2025Article
- Oxidative Stress, Inflammation and Altered Glucose Metabolism Contribute to the Retinal Phenotype in the Choroideremia Zebrafish.Antioxidants (Basel, Switzerland) · 2024Article
- Targeting miR-181a/b in retinitis pigmentosa: implications for disease progression and therapy.Cell & bioscience · 2024Article
- Article
- Txnip deletions and missense alleles prolong the survival of cones in a retinitis pigmentosa mouse model.eLife · 2024Article
- Gene Therapies for Retinitis Pigmentosa that Target Glucose Metabolism.Cold Spring Harbor perspectives in medicine · 2024Review
- The deubiquitinase Otud7b suppresses cone photoreceptor degeneration in mouse models of retinal degenerative diseases.iScience · 2024Article
- CRISPR editing of anti-anemia drug target rescues independent preclinical models of retinitis pigmentosa.Cell reports. Medicine · 2024Article
- Txnip deletions and missense alleles prolong the survival of cones in a retinitis pigmentosa mouse model.bioRxiv : the preprint server for biology · 2024Article
48 more citing papers are in PubMed but not listed here.
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Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
Abstract
Retinitis pigmentosa (RP) is an inherited photoreceptor degenerative disorder that results in blindness. The disease is often caused by mutations in genes that are specific to rod photoreceptors; however, blindness results from the secondary loss of cones by a still unknown mechanism. Here, we demonstrated that the mammalian target of rapamycin complex 1 (mTORC1) is required to slow the progression of cone death during disease and that constitutive activation of mTORC1 in cones is sufficient to maintain cone function and promote long-term cone survival. Activation of mTORC1 in cones enhanced glucose uptake, retention, and utilization, leading to increased levels of the key metabolite NADPH. Moreover, cone death was delayed in the absence of the NADPH-sensitive cell death protease caspase 2, supporting the contribution of reduced NADPH in promoting cone death. Constitutive activation of mTORC1 preserved cones in 2 mouse models of RP, suggesting that the secondary loss of cones is caused mainly by metabolic deficits and is independent of a specific rod-associated mutation. Together, the results of this study address a longstanding question in the field and suggest that activating mTORC1 in cones has therapeutic potential to prolong vision in RP.
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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.