ReviewProgress in retinal and eye research2021
Uncoupling proteins in the mitochondrial defense against oxidative stress.
Review in Progress in retinal and eye research, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 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
57 citing papers in PubMed, 94 citations in OpenAlex.
- Article
- Reduced Cerebral Infarct Volume in Young UCP2Cells · 2026Article
- Suppression of UCP2 alleviates leukemogenesis by enhancing branched-chain amino acids-induced oxidative stress via activating the PI3K/AKT/mTOR signaling pathway.Genes & diseases · 2026Article
- Immunometabolic remodeling of perivascular adipose tissue in murine lupus: implications for lupus vasculopathy.bioRxiv : the preprint server for biology · 2026Article
- Heart-homed nanomedicine induces fast mitochondrial rescue to enhance cardiac function post-myocardial infarction.Bioactive materials · 2026Article
- Mitochondrial protein-enriched artificial nanovesicles: mitochondrial recovery and antioxidation for diabetic wound treatment.Journal of nanobiotechnology · 2026Article
- Deciphering Uncoupling Proteins in Cellular Homeostasis and Metabolic Health.International journal of biological sciences · 2026Review
- Portacaval anastomosis promotes fragmentation of mitochondrial network in the cerebellum of male rats.Metabolic brain disease · 2025Article
- UCP2 inhibition exaggerates diabetic cardiomyopathy by facilitating the activation of NLRP3 and pyroptosis.Diabetology & metabolic syndrome · 2025Article
- Article
- Therapeutic strategies to ameliorate mitochondrial oxidative stress in ischaemia-reperfusion injury: A narrative review.Clinical science (London, England : 1979) · 2025Review
- Irisin regulates oxidative stress and mitochondrial dysfunction through the UCP2-AMPK pathway in prion diseases.Cell death & disease · 2025Article
- Proliferation Inhibited by Genipin in Human Leukemia K562 Cells: Involvement of Uncoupling Protein 2 in Mitochondrial Damage.World journal of oncology · 2025Article
- Targeting Mitochondrial Dysfunction in Cerebral Ischemia: Advances in Pharmacological Interventions.Antioxidants (Basel, Switzerland) · 2025Review
- Volatile oil ofFrontiers in pharmacology · 2025Review
- Bioenergetic-related gene expression in the hippocampus predicts internalizing vs. externalizing behavior in an animal model of temperament.Frontiers in molecular neuroscience · 2025Article
- Interaction between mitochondrial oxidative stress and myocardial fibrosis in the context of diabetes.Frontiers in endocrinology · 2025Review
- Oxidative Stress-related Gene Signature: A Prognostic Tool for Predicting Survival in ST-elevation MI.European cardiology · 2025Article
- Does the Nutrient Adequacy Ratio (NAR) Predict Metabolic Profile and Glycemic Status Among the Obese Population?Nutrition and metabolic insights · 2025Article
- Emerging role and the signaling pathways of uncoupling protein 2 in kidney diseases.Renal failure · 2024Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 2 institutions in 1 country.
Funding
Abstract
Oxidative stress is a major component of most major retinal diseases. Many extrinsic anti-oxidative strategies have been insufficient at counteracting one of the predominant intrinsic sources of reactive oxygen species (ROS), mitochondria. The proton gradient across the inner mitochondrial membrane is a key driving force for mitochondrial ROS production, and this gradient can be modulated by members of the mitochondrial uncoupling protein (UCP) family. Of the UCPs, UCP2 shows a widespread distribution and has been shown to uncouple oxidative phosphorylation, with concomitant decreases in ROS production. Genetic studies using transgenic and knockout mice have documented the ability of increased UCP2 activity to provide neuroprotection in models of a number of diseases, including retinal diseases, indicating that it is a strong candidate for a therapeutic target. Molecular studies have identified the structural mechanism of action of UCP2 and have detailed the ways in which its expression and activity can be controlled at the transcriptional, translational and posttranslational levels. These studies suggest a number of ways in control of UCP2 expression and activity can be used therapeutically for both acute and chronic conditions. The development of such therapeutic approaches will greatly increase the tools available to combat a broad range of serious retinal diseases.
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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.