ReviewFrontiers in molecular biosciences2022
Mutations of CX46/CX50 and Cataract Development.
Review in Frontiers in molecular biosciences, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 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
12 citing papers in PubMed, 23 citations in OpenAlex.
- Identification of Variants in Two Families With Congenital Cataract by Whole Exome Sequencing.Molecular genetics & genomic medicine · 2026Article
- Connexin50 hemichannels are opened by COFrontiers in physiology · 2026Article
- Connexin Restrains EMT by Dual-Domain Mechanisms to Preserve Epithelial Identity.Research square · 2025Article
- Identification of co-segregatingFrontiers in medicine · 2025Article
- Oxidative Stress in Cataract Formation: Is There a Treatment Approach on the Horizon?Antioxidants (Basel, Switzerland) · 2024Review
- Altered Cell Clusters and Upregulated Aqp1 in Connexin 50 Knockout Lens Epithelium.Investigative ophthalmology & visual science · 2024Article
- Oxidative Stress and Cataract Formation: Evaluating the Efficacy of Antioxidant Therapies.Biomolecules · 2024Review
- JAM-C Is Important for Lens Epithelial Cell Proliferation and Lens Fiber Maturation in Murine Lens Development.Investigative ophthalmology & visual science · 2023Article
- Gene profiles and mutations in the development of cataracts in the ICR rat model of hereditary cataracts.Scientific reports · 2023Article
- Protein kinase A activation alleviates cataract formation via increased gap junction intercellular communication.iScience · 2023Article
- A Quantitative Assay for CaInternational journal of molecular sciences · 2022Article
- Beyond the Channels: Adhesion Functions of Aquaporin 0 and Connexin 50 in Lens Development.Frontiers in cell and developmental biology · 2022Review
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cataract is a common disease in the aging population. Gap junction has been considered a central component in maintaining homeostasis for preventing cataract formation. Gap junction channels consist of connexin proteins with more than 20 members. Three genes including GJA1, GJA3, and GJA8, that encode protein Cx43 (connexin43), Cx46 (connexin46), and Cx50 (connexin50), respectively, have been identified in human and rodent lens. Cx46 together with Cx50 have been detected in lens fiber cells with high expression, whereas Cx43 is mainly expressed in lens epithelial cells. Disrupted expression of the two connexin proteins Cx46 and Cx50 is directly related to the development of severe cataract in human and mice. In this review article, we describe the main role of Cx46 and Cx50 connexin proteins in the lens and the relationship between mutations of Cx46 or Cx50 and hereditary cataracts. Furthermore, the latest progress in the fundamental research of lens connexin and the mechanism of cataract formation caused by lens connexin dysfunction are summarized. Overall, targeting connexin could be a novel approach for the treatment of cataract.
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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.