ReviewInternational journal of molecular sciences2024
The Synergistic Effects of Polyol Pathway-Induced Oxidative and Osmotic Stress in the Aetiology of Diabetic Cataracts.
Review in International journal of molecular sciences, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers, 1 of them a synthesis that pooled it.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
25 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Expression and mechanistic roles of long non-coding RNAs in diabetic cataract: a systematic review and meta-analysis.Biology direct · 2026Pooled it
- Article
- Cataract GWAS meta-analysis and multi-omics Mendelian randomisation inform disease mechanisms and candidate target prioritisation.EBioMedicine · 2026Article
- Antioxidants in Oxidative Stress and Obesity-Associated Diseases: Molecular Mechanisms and Potential Health Implications.Biomedicines · 2026Review
- A Systems View of Posterior Capsule Opacification: TGF-β/ROS Signaling, Mitochondrial Homeostasis, and Injury/Aging Cues-Therapeutic Opportunities.Investigative ophthalmology & visual science · 2026Review
- Comorbidities in Age-Related Cataract: Epidemiological Burden and Public Health Implications.Vision (Basel, Switzerland) · 2026Review
- USP10 inhibits the apoptosis of lens epithelial cells and delays the progression of diabetic cataract via the deubiquitination and stabilization of MCL1.Scientific reports · 2026Article
- PANK4 Regulates YAP to Modulate the Glycolytic Pathway in LEC for Driving LECs-EMT in Early Diabetic Cataract Pathogenesis.Investigative ophthalmology & visual science · 2026Article
- Improving Photosynthetic Efficiency and Biochemical Adaptations in Tomatoes under Drought Stress through Seaweed Aqueous Extract Application.ACS omega · 2026Article
- Inflammation-Mediated Immune Imbalance in the Pathogenesis of Diabetic Cataracts.Biomedicines · 2026Article
- The NFAT5-AR Axis Is Associated with Hyperosmolarity, Renal Dysfunction, and Neutrophil-Related Inflammatory Markers in Diabetic Retinopathy.International journal of molecular sciences · 2026Article
- Gigantol Preserves Lens Biophysical Homeostasis by Restoring Cytoskeletal Integrity and Membrane Fluidity in a Diabetic Cataract Model.International journal of molecular sciences · 2026Article
- Lactate dehydrogenase A exhibits sorbitol/fructose-related catalytic activity and contributes to polyol pathway metabolism in tumor cells.Frontiers in endocrinology · 2026Article
- New Insight Into Male Infertility: Deviation From Basic Tenets of Life.Oxidative medicine and cellular longevity · 2026Review
- Clinical Importance of miRNA in Diabetic Neuropathy: Pathophysiology, Diagnosis, and Therapeutic Potential.Current diabetes reviews · 2026Review
- Lens epithelial cells senescence in cataract pathogenesis and emerging therapeutic opportunities.Frontiers in cell and developmental biology · 2026Review
- Glutaredoxin 2 Protects Lens Epithelial Cells From Ferroptosis by Preventing HNRNPA2B1 S-Glutathionylation in Diabetes-Mediated Cataractogenesis.Investigative ophthalmology & visual science · 2025Article
- Aldose Reductase Involvement in EMT: Emerging Insights and Current Proposed Molecular Mechanisms.Biology · 2025Review
- Plumbagin Protects Diabetogenic Cataract Formation by Mitigating Lens Aldose Reductase and Oxidative Stress.Journal of pharmacopuncture · 2025Article
- Pathophysiological Mechanisms of Diabetes-Induced Macrovascular and Microvascular Complications: The Role of Oxidative Stress.Medical sciences (Basel, Switzerland) · 2025Review
Corrections and comments
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Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cataracts are the world's leading cause of blindness, and diabetes is the second leading risk factor for cataracts after old age. Despite this, no preventative treatment exists for cataracts. The altered metabolism of excess glucose during hyperglycaemia is known to be the underlying cause of diabetic cataractogenesis, resulting in localised disruptions to fibre cell morphology and cell swelling in the outer cortex of the lens. In rat models of diabetic cataracts, this damage has been shown to result from osmotic stress and oxidative stress due to the accumulation of intracellular sorbitol, the depletion of NADPH which is used to regenerate glutathione, and the generation of fructose metabolites via the polyol pathway. However, differences in lens physiology and the metabolism of glucose in the lenses of different species have prevented the translation of successful treatments in animal models into effective treatments in humans. Here, we review the stresses that arise from hyperglycaemic glucose metabolism and link these to the regionally distinct metabolic and physiological adaptations in the lens that are vulnerable to these stressors, highlighting the evidence that chronic oxidative stress together with osmotic stress underlies the aetiology of human diabetic cortical cataracts. With this information, we also highlight fundamental gaps in the knowledge that could help to inform new avenues of research if effective anti-diabetic cataract therapies are to be developed in the future.
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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.