ArticleScientific reports2020
Polymorphisms in miRNA binding sites involved in metabolic diseases in mice and humans.
Article in Scientific reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 16 citations in OpenAlex.
- Loss of miRNA-Mediated VEGFA Regulation by SNP-Induced Impairment: A Bioinformatic Analysis in Diabetic Complications.Biomedicines · 2025Article
- microRNAs in Type 1 Diabetes: Roles, Pathological Mechanisms, and Therapeutic Potential.International journal of molecular sciences · 2025Review
- Article
- Childhood obesity, metabolic syndrome, and oxidative stress: microRNAs go on stage.Reviews in endocrine & metabolic disorders · 2023Review
- Identification of MicroRNAs Associated with Prediabetic Status in Obese Women.International journal of molecular sciences · 2023Article
- Hypoxia-induced PPFIA4 accelerates the progression of ovarian cancer through glucose metabolic reprogramming.Medical oncology (Northwood, London, England) · 2023Article
- PPFIA4 promotes castration-resistant prostate cancer by enhancing mitochondrial metabolism through MTHFD2.Journal of experimental & clinical cancer research : CR · 2022Article
- TOX4, an insulin receptor-independent regulator of hepatic glucose production, is activated in diabetic liver.Cell metabolism · 2022Article
- Regulation of KRAS protein expression by miR-544a and KRAS-LCS6 polymorphism in wild-type KRAS sporadic colon adenocarcinoma.Human cell · 2021Article
- PPFIA4 Promotes Colon Cancer Cell Proliferation and Migration by Enhancing Tumor Glycolysis.Frontiers in oncology · 2021Article
- Involvement of miR-142 and miR-155 in Non-Infectious Complications of CVID.Molecules (Basel, Switzerland) · 2020Review
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Authors and funding
7 authors at 6 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Type 2 diabetes and obesity are well-studied metabolic diseases, which are based on genetic and epigenetic alterations in combination with an obesogenic lifestyle. The aim of this study was to test whether SNPs in miRNA-mRNA binding sites that potentially disrupt binding, elevate the expression of miRNA targets, which participate in the development of metabolic diseases. A computational approach was developed that integrates transcriptomics, linkage analysis, miRNA-target prediction data, and sequence information of a mouse model of obesity and diabetes. A statistical analysis demonstrated a significant enrichment of 566 genes for a location in obesity- and diabetes-related QTL. They are expressed at higher levels in metabolically relevant tissues presumably due to altered miRNA-mRNA binding sites. Of these, 51 genes harbor conserved and impaired miRNA-mRNA-interactions in human. Among these, 38 genes have been associated to metabolic diseases according to the phenotypes of corresponding knockout mice or other results described in the literature. The remaining 13 genes (e.g. Jrk, Megf9, Slfn8 and Tmem132e) could be interesting candidates and will be investigated in the future.
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