ReviewFree radical biology & medicine2021
The stress response protein REDD1 as a causal factor for oxidative stress in diabetic retinopathy.
Review in Free radical biology & medicine, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
22 citing papers in PubMed, 33 citations in OpenAlex.
- Hippocampal REDD1 inhibition is critical for alleviating depressive-like behaviors.Acta pharmacologica Sinica · 2026Article
- Prostaglandin E2 alleviates acetaminophen-induced liver injury through DDIT4-enhanced autophagy regulated by circLima1/miR-486.Scientific reports · 2026Article
- SIX2-Mediated Microglial M2 Polarization and Exosomal miR-3470b Delivery Protect Dopaminergic Neurons in Parkinson's Disease.CNS neuroscience & therapeutics · 2026Article
- Freeze-Dried Extracts ofPreventive nutrition and food science · 2026Article
- Exploring the protective role of DDIT4/mTOR in podocyte integrity through macrophage polarization in diabetic kidney disease.Renal failure · 2025Article
- Review
- Single-cell transcriptomics of neuroinflammation and cerebrovascular endothelial cells in the aged rat hippocampus.iScience · 2025Article
- Identification of potential anti aging drugs and targets in chronic kidney disease.Scientific reports · 2025Article
- Deletion of the stress response protein REDD1 prevents sodium iodate-induced RPE damage and photoreceptor loss.GeroScience · 2025Article
- Podocyte-Specific Expression of the Stress Response Protein REDD1 Is Necessary for Diabetes-Induced Podocytopenia.Diabetes · 2025Article
- Identification and validation of integrated stress-response-related genes as biomarkers for age-related macular degeneration.Frontiers in molecular biosciences · 2025Article
- Review
- Mechanisms driving fasting-induced protection from genotoxic injury in the small intestine.American journal of physiology. Gastrointestinal and liver physiology · 2024Article
- Unraveling DDIT4 in the VDR-mTOR pathway: a novel target for drug discovery in diabetic kidney disease.Frontiers in pharmacology · 2024Article
- Phytocannabinoids as Potential Multitargeting Neuroprotectants in Alzheimer's Disease.Current drug research reviews · 2024Review
- Alleviate oxidative stress in diabetic retinopathy: antioxidant therapeutic strategies.Redox report : communications in free radical research · 2023Review
- The stress-responsive protein REDD1 and its pathophysiological functions.Experimental & molecular medicine · 2023Review
- Activation of Disulfide Redox Switch in REDD1 Promotes Oxidative Stress Under Hyperglycemic Conditions.Diabetes · 2022Article
- Blueberry Anthocyanins from Commercial Products: Structure Identification and Potential for Diabetic Retinopathy Amelioration.Molecules (Basel, Switzerland) · 2022Article
- Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Diabetic Retinopathy (DR) is a major cause of visual dysfunction, yet much remains unknown regarding the specific molecular events that contribute to diabetes-induced retinal pathophysiology. Herein, we review the impact of oxidative stress on DR, and explore evidence that supports a key role for the stress response protein regulated in development and DNA damage (REDD1) in the development of diabetes-induced oxidative stress and functional defects in vision. It is well established that REDD1 mediates the cellular response to a number of diverse stressors through repression of the central metabolic regulator known as mechanistic target of rapamycin complex 1 (mTORC1). A growing body of evidence also supports that REDD1 acts independent of mTORC1 to promote oxidative stress by both enhancing the production of reactive oxygen species and suppressing the antioxidant response. Collectively, there is strong preclinical data to support a key role for REDD1 in the development and progression of retinal complications caused by diabetes. Furthermore, early proof-of-concept clinical trials have found a degree of success in combating ischemic retinal disease through intravitreal delivery of an siRNA targeting the REDD1 mRNA. Overall, REDD1-associated signaling represents an intriguing target for novel clinical therapies that go beyond addressing the symptoms of diabetes by targeting the underlying molecular mechanisms that contribute to DR.
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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.