ArticlePloS one2025
G91-deletion in βA3/A1-crystallin induces cellular and molecular changes in mouse lenses leading to congenital cataract development.
Article in PloS one, 2025. 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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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.
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Who cites it
2 citing papers in PubMed.
- A Novel CRYBB2 Splicing Mutation Is Associated With Lens Extracellular Matrix Remodeling and Vascular Alterations in Congenital Cataract.Investigative ophthalmology & visual science · 2026Article
- Identification and functional characterization of a novel CRYBB1 deletion mutation causing autosomal dominant congenital cataract in a Chinese family.BMC ophthalmology · 2026Article
Corrections and comments
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Authors and funding
3 authors.
Funding
Abstract
CRYβA1-ΔG91 (βA3ΔG91) is a mutational hotspot in CRYβA1, which causes autosomal dominant congenital nuclear cataract in humans and mice. Previous in-vitro studies of recombinant βA3ΔG91 showed defective folding, decreased solubility, and aberrant oligomerization of βA3ΔG91 with other crystallins. Emerging evidence demonstrates an association between autophagy and βA3ΔG91-induced congenital cataracts. To gain further understanding of the molecular mechanism of congenital cataract development in βA3ΔG91 mice, we examined the βA3ΔG91- vs WT- lenses for complete gene profiling, lens epithelial cell (LEC) proliferation and migration, and lens epithelial-fiber cell differentiation. We also determined the changes in crystallin proteomic profiles in water-soluble, water-insoluble-urea-soluble, and water-insoluble-urea-insoluble fractions. Our results show that relative to WT lenses, the βA3ΔG91 lenses showed: (A) downregulation of genes associated with LECs proliferation and migration (B) abnormal suture line pattern, (C) significant reduction in proliferation and migration of LECs, (D) abnormal F-actin distribution, (E) increased high molecular weight (HMW) peak, and (F) insolubilization and degradation of crystallins and other lens proteins. Together, these defects contribute to the formation of the lens opacity in βA3ΔG91 mice lenses.
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Registered trials
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