ArticleCell death discovery2024
Uric acid-driven NLRP3 inflammasome activation triggers lens epithelial cell senescence and cataract formation.
Article in Cell death discovery, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 14 citations in OpenAlex.
- Association of serum uric acid with circulating inflammatory proteins and treatment response to ixekizumab in patients with psoriasis: A multicenter prospective cohort study in China.Chinese medical journal · 2026Trial
- Dietary and Formulation Potential of Natural Oils and Fats in Ocular Health and Disease: Mechanisms, Evidence, and Future Directions.Nutrients · 2026Review
- SERSome-based metabolic profiling of aqueous humor for cataract subtyping with molecule-level interpretability.Journal of nanobiotechnology · 2026Article
- A three-pronged strategy with minimalist nattokinase nanocomposite eye drops breaks the vicious cycle in ultraviolet-B-induced cataract.Journal of nanobiotechnology · 2026Article
- Association between serum uric acid level and cataract Arisk: A cross-sectional study based on two databases (CHARLS and NHANES).The Journal of international medical research · 2026Article
- Correlation between hyperuricemia and coronary artery calcification.The Journal of international medical research · 2026Review
- Loss of Peroxiredoxin 6 Drives Age-Related Klf9/NF-Antioxidants (Basel, Switzerland) · 2026Article
- Cellular Senescence of Lens Epithelial Cells and Age-Related Cataract: A Systematic Review.Bioengineering (Basel, Switzerland) · 2026Review
- Lens aging and disease: Molecular mechanisms, functional consequences, and pharmacological implications.Progress in retinal and eye research · 2026Review
- Lens epithelial cells senescence in cataract pathogenesis and emerging therapeutic opportunities.Frontiers in cell and developmental biology · 2026Review
- Astragaloside IV Alleviates Fructose-Induced Intestinal Metabolic Senescence by Targeting Ketohexokinase Asn261/Ala226 to Preserve Intestinal Stem Cell Homeostasis.ACS central science · 2025Article
- Lens Proteomics Provide Novel Clues for Cataractogenesis: Original Investigation and a Broad Literature Survey.Journal of clinical medicine · 2025Article
- Review
- 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
- Assessing the relationship between gout and the risk of cataract in community-dwelling older adults: mediation and moderation analysis.Frontiers in medicine · 2025Article
- Efficacy evaluation and predictive value of IL-20 and Apelin-13 after cataract surgery by phacoemulsification combined with IOL implantation.Frontiers in medicine · 2025Article
- Gout and Hyperuricemia: A Narrative Review of Their Comorbidities and Clinical Implications.Journal of clinical medicine · 2024Review
- The impact of alternate-day fasting on the salivary gland stem cell compartments in non-obese diabetic mice with newly established Sjögren's syndrome.Biochimica et biophysica acta. Molecular cell research · 2024Article
Corrections and comments
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Authors and funding
9 authors at 5 institutions in 3 countries.
Funding
Abstract
Excessive uric acid (UA) is associated with age-related cataract. A previous study showed that a high UA level in the aqueous humor stimulated the senescence of lens epithelial cells (LECs), leading to cataract progression. To better understand the underlying mechanisms, we investigated UA-driven senescence in human lens tissue samples obtained during surgery, rat lens organ cultures, and in vivo experiments, using senescence-associated β-galactosidase (SA-β-gal) staining, electronic microscopy, Western blotting, and histological analyses. Initially, we identified markedly higher expressions of NLRP3 and caspase-1 in the lens capsules of hyper-uricemic patients compared to normo-uricemic patients. This increase was accompanied by a significant rise in the SA-β-gal positive rate. We next built a cataract model in which rat lenses in an organ culture system were treated with an increasing dosage of UA. Notably, opacification was apparent in the lenses treated with 800 μM of UA starting on the fifth day. Mechanistically, UA treatment not only significantly induced the expression of NLRP3, caspase-1, and IL-1β, but also upregulated the levels of SA-β-gal and the senescence regulators p53 and p21. These effects were fully reversed, and lens opacification was ameliorated by the addition of MCC950, a selective NLRP3 antagonist. Moreover, an in vivo model showed that intravitreal UA injection rapidly induced cataract phenotypes within 21 days, an effect significantly mitigated by co-injection with MCC950. Together, our findings suggest that targeting the UA-induced NLRP3 inflammasome with MCC950 could be a promising strategy for preventing cataract formation associated with inflammageing.
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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.