ArticleMolecular medicine reports2017
Investigation of the molecular mechanisms underlying myotonic dystrophy types 1 and 2 cataracts using microRNA‑target gene networks.
Article in Molecular medicine reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed, 5 citations in OpenAlex.
- Integrative transcriptomic profiling of ncRNAs and mRNAs in developing mouse lens.Frontiers in genetics · 2024Article
- Transcriptome Analysis Reveals Altered Inflammatory Pathway in an Inducible Glial Cell Model of Myotonic Dystrophy Type 1.Biomolecules · 2021Article
- Core Clinical Phenotypes in Myotonic Dystrophies.Frontiers in neurology · 2018Review
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The purpose of the present study was to investigate the molecular mechanisms of myotonic dystrophy (DM) 1 and 2 cataracts using bioinformatics methods. A microarray dataset (E‑MEXP‑3365) downloaded from the Array Express database included lens epithelial samples of DM1 and DM2 cataract patients (n=3/group) and non‑DM lens epithelial samples as a control (n=4). Differentially expressed genes (DEGs) were identified between DM1 and control samples, and between DM2 and control samples. Pathway enrichment analyses were performed for the DEGs. Potential micro (mi)RNAs regulating these DEGs were predicted. An miRNA‑target gene network was constructed for DM1 and DM2. The study identified 223 DEGs in DM1, and 303 DEGs in DM2. DM1 and DM2 shared 172 DEGs. The DEGs in DM1 were enriched with calcium, Wnt and axon guidance signaling pathways. The DEGs in DM2 were linked by adherens junction signaling pathways. miRNA (miR)‑197, miR‑29b and miR‑29c were included in the network modules of DM1. miR‑197, miR‑29c and miR‑29a were involved in the network modules of DM2. It is therefore hypothesized that these signaling pathways and miRNAs underlie DM1 and DM2 cataracts, and may represent potential therapeutic targets for the treatment of this disorder.
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