ArticleInternational journal of molecular sciences2023
Synergic Action of Insulin-like Growth Factor-2 and miRNA-483 in Pterygium Pathogenesis.
Article in International journal of molecular sciences, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
What it found
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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
7 citing papers in PubMed, 10 citations in OpenAlex.
- miR-381-3p suppresses pterygium progression by regulating HACE1/TRIP12-mediated ubiquitin-degradation of MCPIP1.In vitro cellular & developmental biology. Animal · 2026Article
- Oral Microbiota Taxa and Pri-miRNA Expression in Bipolar Disorder: A Case-Control Study.Biomolecules · 2025Article
- Advances of IGF-1R inhibitors in Graves' ophthalmopathy.International ophthalmology · 2024Review
- Prostate-specific antigen: An unfamiliar protein in the human salivary glands.Journal of anatomy · 2024Article
- The role of oxidative stress in the pathogenesis of ocular diseases: an overview.Molecular biology reports · 2024Review
- Dysfunction in IGF2R Pathway and Associated Perturbations in Autophagy and WNT Processes in Beckwith-Wiedemann Syndrome Cell Lines.International journal of molecular sciences · 2024Article
- Review
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Authors and funding
9 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Pterygium is a multifactorial disease in which UV-B is speculated to play a key role by inducing oxidative stress and phototoxic DNA damage. In search for candidate molecules that are useful for justifying the intense epithelial proliferation observed in pterygium, our attention has been focused on Insulin-like Growth Factor 2 (IGF-2), mainly detected in embryonic and fetal somatic tissues, which regulate metabolic and mitogenic functions. The binding between IGF-2 and its receptor Insulin-like Growth Factor 1 Receptor (IGF-1R) activates the PI3K-AKT pathway, which leads to the regulation of cell growth, differentiation, and the expression of specific genes. Since IGF2 is regulated by parental imprinting, in different human tumors, the IGF2 Loss of Imprinting (LOI) results in IGF-2- and IGF2-derived intronic miR-483 overexpression. Based on these activities, the purpose of this study was to investigate the overexpression of IGF-2, IGF-1R, and miR-483. Using an immunohistochemical approach, we demonstrated an intense colocalized epithelial overexpression of IGF-2 and IGF-1R in most pterygium samples (Fisher's exact test,
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Registered trials
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