ArticleInvestigative ophthalmology & visual science2024
UCP2-SIRT3 Signaling Relieved Hyperglycemia-Induced Oxidative Stress and Senescence in Diabetic Retinopathy.
Article in Investigative ophthalmology & visual science, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 16 citations in OpenAlex.
- Identification and analysis of oxidative stress-related genes associated with the occurrence and development of diabetic retinopathy.Scientific reports · 2026Article
- Dual-Target ROS-Driven Spatiotemporal Senolysis for Vascular Repair and Immune Microenvironment Reprogramming in the Treatment of Ocular Fundus Neovascularization.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- miR-329-3p in Bone Marrow Mesenchymal Stem Cells-Derived Exosomes Promotes Bone Regeneration in Diabetic Fractures by Alleviating the SIRT3-Mediated Oxidative Stress via Inhibiting LSD1.Stem cells international · 2026Article
- Fluconazole-Decorated Gold Nanoparticles as a Novel Therapeutic Strategy Against Carbapenem-ResistantInfection and drug resistance · 2026Article
- Article
- Breakthroughs in diabetic retinopathy diagnosis and treatment using preclinical research models: current progress and future directions.Annals of medicine · 2025Review
- Recent advances in engineered exosome-based therapies for ocular vascular disease.Journal of nanobiotechnology · 2025Review
- Mitochondria in oxidative stress, inflammation and aging: from mechanisms to therapeutic advances.Signal transduction and targeted therapy · 2025Review
- The Role of Endothelial Senescence in the Pathogenesis of Diabetic Retinopathy.International journal of molecular sciences · 2025Review
- Roxadustat improves diabetic myocardial injury by upregulating HIF-1α/UCP2 against oxidative stress.Cardiovascular diabetology · 2025Article
- Targeting senescence to prevent diabetic kidney disease: Exploring molecular mechanisms and potential therapeutic targets for disease management.Diabetic medicine : a journal of the British Diabetic Association · 2025Review
- Diagnostic and Prognostic Predictive Value of Serum Selenium and Redox Biomarkers in Retinal Vein Occlusion.International journal of general medicine · 2025Article
- METTL3 blocked the progression of diabetic retinopathy through m6A-modified SOX2.Open medicine (Warsaw, Poland) · 2025Article
- SIRT3 is required for the protective function of ketogenic diet on neural inflammation and neuropathic pain.International journal of biological sciences · 2025Article
- Resilience to diabetic retinopathy.Progress in retinal and eye research · 2024Review
Corrections and comments
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Authors and funding
10 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Purpose: Diabetic retinopathy (DR) is one of the most common reasons for blindness. uncoupling protein 2 (UCP2), an uncoupling protein located in mitochondria, has been reported to be related to metabolic and vascular diseases. This research aimed to illustrate the function and mechanism of UCP2 in the pathogenesis of DR. Methods: Human epiretinal membranes were collected to investigate the expression of UCP2 by quantitative real-time polymerase chain reaction (qRT-PCR) and immunofluorescence. Primary human retinal microvascular endothelial cells (HRECs) were cultured in high glucose (HG) to establish an in vitro cell model for DR. Flow cytometry analysis was used to measure intracellular reactive oxygen species (ROS). Senescence levels were evaluated by the senescence-associated beta-galactosidase (SA-β-gal) assay, the expression of senescence marker P21, and cell-cycle analysis. Adenovirus-mediated UCP2 overexpression or knockdown and specific inhibitors were administered to investigate the underlying regulatory mechanism. Results: Proliferative fibrovascular membranes from patients with DR illustrated the downregulation of UCP2 and sirtuin 3 (SIRT3) by qRT-PCR and immunofluorescence. Persistent hyperglycemia-induced UCP2 downregulation in the progress of DR and adenovirus-mediated UCP2 overexpression protected endothelial cells from hyperglycemia-induced oxidative stress and senescence. Under hyperglycemic conditions, UCP2 overexpression attenuated NAD+ downregulation; hence, it promoted the expression and activity of SIRT3, an NAD+-dependent deacetylase regulating mitochondrial function. 3-TYP, a selective SIRT3 inhibitor, abolished the UCP2-mediated protective effect against oxidative stress and senescence. Conclusions: UCP2 overexpression relieved oxidative stress and senescence based on a novel mechanism whereby UCP2 can regulate the NAD+-SIRT3 axis. Targeting oxidative stress and senescence amelioration, UCP2-SIRT3 signaling may serve as a method for the prevention and treatment of DR and other diabetic vascular diseases.
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