ArticleClinical ophthalmology (Auckland, N.Z.)2016
Silent information regulator T1 in aqueous humor of patients with cataract.
Article in Clinical ophthalmology (Auckland, N.Z.), 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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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.
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Who cites it
2 citing papers in PubMed, 7 citations in OpenAlex.
- Metformin attenuates TBHP-induced oxidative injury in human lens epithelial cells and is associated with SIRT1/FOXO1-related autophagy.PloS one · 2026Article
- Expression of miR-34a in cataract rats and its related mechanism.Experimental and therapeutic medicine · 2020Article
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
purposeSilent information regulator T1 (SIRT1), a member of the sirtuin family, has a preventive role in various ocular diseases. We evaluated the relations between the aqueous humor level of SIRT1 and age, sex, systemic diseases, the severity of lens opacity, and other factors.
settingThis study was conducted at a university teaching hospital in Tokyo, Japan.
designThis study was designed based on the consecutive case series.
methodsAqueous humor samples were obtained from 29 eyes of the 21 consecutive patients undergoing surgery for age-related cataract (ARC). SIRT1 levels were determined by enzyme-linked immunosorbent assay.
resultsAqueous humor levels of SIRT1 showed a positive correlation with visual acuity (logarithm of the minimum angle of resolution) and with the severity of nuclear cataract (r=0.32 and 0.30, respectively, P<0.05). However, only visual acuity was correlated with SIRT1 according to the stepwise multiple regression analysis (P<0.05).
conclusionThese findings suggest that SIRT1 may have an effect on the formation of ARC, acting as a defensive factor against ARC.
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