ArticleFASEB journal : official publication of the Federation of American Societies for Experimental Biology2018
Deletion of the stress-response protein REDD1 promotes ceramide-induced retinal cell death and JNK activation.
Article in FASEB journal : official publication of the Federation of American Societies for Experimental Biology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
What it found
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Who cites it
20 citing papers in PubMed, 25 citations in OpenAlex.
- Hippocampal REDD1 inhibition is critical for alleviating depressive-like behaviors.Acta pharmacologica Sinica · 2026Article
- GSK3β promotes p53/Nrf2-dependent expression of the stress response protein REDD2 in retinal Müller glia exposed to hyperlipidemic conditions.Experimental eye research · 2026Article
- REDD1/DDIT4 counteracts endoplasmic reticulum stress-induced apoptosis by controlling the expression of death receptor TRAILR2/DR5 in cancer cells.Cell death & disease · 2026Article
- High-fat diet alters retinal lipid composition and gene expression networks in mice.BMC biology · 2025Article
- Elevated Very-Long-Chain Ceramides in the Vitreous Humor of Patients With Proliferative Diabetic Retinopathy.Investigative ophthalmology & visual science · 2025Article
- Review
- NLRP3 Inflammasome Priming in the Retina of Diabetic Mice Requires REDD1-Dependent Activation of GSK3β.Investigative ophthalmology & visual science · 2024Article
- The stress-responsive protein REDD1 and its pathophysiological functions.Experimental & molecular medicine · 2023Review
- MicroRNA-based engineering of mesenchymal stem cell extracellular vesicles for treatment of retinal ischemic disorders: Engineered extracellular vesiclesand retinal ischemia.Acta biomaterialia · 2023Article
- PERK/ATF4-dependent expression of the stress response protein REDD1 promotes proinflammatory cytokine expression in the heart of obese mice.American journal of physiology. Endocrinology and metabolism · 2023Article
- Activation of Disulfide Redox Switch in REDD1 Promotes Oxidative Stress Under Hyperglycemic Conditions.Diabetes · 2022Article
- Article
- Müller Glial Expression of REDD1 Is Required for Retinal Neurodegeneration and Visual Dysfunction in Diabetic Mice.Diabetes · 2022Article
- Thioredoxin interacting protein, a key molecular switch between oxidative stress and sterile inflammation in cellular response.World journal of diabetes · 2021Review
- Emerging Targets in Type 2 Diabetes and Diabetic Complications.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2021Review
- Impacts of high fat diet on ocular outcomes in rodent models of visual disease.Experimental eye research · 2021Review
- The stress response protein REDD1 as a causal factor for oxidative stress in diabetic retinopathy.Free radical biology & medicine · 2021Review
- The stress response protein REDD1 promotes diabetes-induced oxidative stress in the retina by Keap1-independent Nrf2 degradation.The Journal of biological chemistry · 2020Article
- REDD1 Activates a ROS-Generating Feedback Loop in the Retina of Diabetic Mice.Investigative ophthalmology & visual science · 2019Article
- Consumption of a high fat diet promotes protein O-GlcNAcylation in mouse retina via NR4A1-dependent GFAT2 expression.Biochimica et biophysica acta. Molecular basis of disease · 2018Article
Corrections and comments
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
Abstract
The role of dyslipidemia in the development of retinal dysfunction remains poorly understood. Using an animal model of diet-induced obesity/pre-type 2 diabetes, we investigated molecular defects in the retina arising from consumption of a diet high in saturated fats and sugars ( i.e., a Western diet). We found that feeding mice a Western diet increased the abundance of retinal sphingolipids, attenuated protein kinase B (Akt) phosphorylation, enhanced JNK activation, and increased retinal cell death. When we used palmitate or C6-ceramide (Cer) to assess sphingolipid-mediated signaling in cultured murine and human cells, we observed similar effects on Akt, JNK, and cell death. Furthermore, both Western diet and C6-Cer exposure enhanced expression of the stress-response protein regulated in development and DNA damage response 1 (REDD1) and loss of REDD1 increased C6-Cer-induced JNK activation and cell death. Exogenous REDD1 expression repressed JNK-mediated phosphorylation in cultured cells. We found that thioredoxin-interacting protein (TXNIP) expression was elevated in REDD1-deficient cell lines and C6-Cer promoted TXNIP expression in both wild-type and REDD1-deficient cells. Likewise, TXNIP knockdown attenuated JNK activation and caspase 3 cleavage after either C6-Cer exposure or REDD1 deletion. The results support a model wherein Cer-induced REDD1 expression attenuates TXNIP-dependent JNK activation and retinal cell death.-Dai, W., Miller, W. P., Toro, A. L., Black, A. J., Dierschke, S. K., Feehan, R. P., Kimball, S. R., Dennis, M. D. Deletion of the stress-response protein REDD1 promotes ceramide-induced retinal cell death and JNK activation.
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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 Socratic graph.