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PubMed · 8302525

Evaluating visual function in cataract.

D B Elliott
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Abstract

This paper reviews recent research on the evaluation of visual function in cataract. Visual impairment in cataract is principally caused by increased intraocular forward light scatter. It is assumed that visual acuity (VA) measurements assess the impact of narrow angle light scatter. This also makes the measurement of high spatial frequency contrast sensitivity (CS) unnecessary. However, VA measurements alone are an inadequate assessment of visual impairment in some patients with cataract. In addition, it is suggested that a measurement of wide-angle light scatter is required. This can be evaluated directly using the van den Berg Straylightmeter, or indirectly using low spatial frequency CS or disability glare (DG) tests. The following are discussed: (1) the relative usefulness of these tests; (2) how they can be incorporated into the decision as to when to extract a cataract; and (3) the importance of considering binocular visual function.

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CataractCataract ExtractionContrast SensitivityEvaluation Studies as TopicHumansLens, CrystallineLightScattering, RadiationVision TestsVision, OcularVisual AcuityJournal ArticleResearch Support, Non-U.S. Gov'tReview

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BibTeXRIS

D B Elliott. 1993. Evaluating visual function in cataract.. https://doi.org/10.1097/00006324-199311000-00006

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KLF5 promotes proliferation, migration, and autophagy-/EMT‑associated molecular changes in lens epithelial cells via transcriptional activation of THBS1 in traumatic cataract.

PURPOSE: Traumatic cataract is a common blinding eye disease after ocular trauma, and its pathogenesis is closely related to lens epithelial cell dysfunction, while the definite molecular regulatory mechanism between upstream transcription factor and downstream target gene remains poorly clarified. This study aimed to clarify the role and molecular mechanism of the krüppel-like factor 5 (KLF5)/ thrombosponin 1 (THBS1) axis in regulating proliferation, migration, epithelial-mesenchymal transition and autophagy of lens epithelial cells in traumatic cataract, and to explore its potential clinical therapeutic value. METHODS: The GSE295383 dataset in the gene expression omnibus (GEO) database was downloaded, and the differentially expressed genes (DEGs) were screened by linear models for microarray data (limma) package of R language. Combined with Weighted gene co-expression network analysis (WGCNA), the gene co-expression network was constructed and the key modules were screened. Gene ontology (GO), kyoto encyclopedia of genes and genomes (KEGG) and gene set enrichment analysis (GSEA) combined with human transcription factor target (hTFtarget) and JASPAR databases were used to predict the upstream transcription factors of THBS1. Subsequently, SRA01/04 cells were induced with transforming growth factor-beta 2 (TGF-β2) to construct a cataract cell model. RESULTS: THBS1 and KLF5 were highly expressed in LECs exposed to TGF-β2. KLF5 could activate THBS1 transcription by binding to THBS1 promoter - 174 to -165 sites. Knockdown of THBS1 inhibited TGF-β2-induced viability, proliferation, migration, and altered the expression of epithelial-mesenchymal transition (EMT)- and autophagy-related markers in LECs. Knockdown of KLF5 downregulated THBS1 expression and produced a similar inhibitory effect, while overexpression of THBS1 reversed the effect of KLF5 knockdown. CONCLUSIONS: This study demonstrated that KLF5 promoted the proliferation, migration, and EMT‑associated molecular changes of LECs in traumatic cataract through transcriptional activation of THBS1, and regulated the expression of autophagy‑related markers in LECs, suggesting that KLF5/THBS1 axis might be a potential target for the treatment of traumatic cataract.

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