دورية أكاديمية
Pathogenic gene connections in type 2 diabetes and non-alcoholic fatty liver disease: a bioinformatics analysis and mouse model investigations experiments.
العنوان: | Pathogenic gene connections in type 2 diabetes and non-alcoholic fatty liver disease: a bioinformatics analysis and mouse model investigations experiments. |
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المؤلفون: | Chen C; Institute of Genomics, School of Medicine, Huaqiao University, 668 Jimei Road, Xiamen, 361021, China. chenchao@hqu.edu.cn., Yang K; School of Medicine, Xiamen University, Xiamen, 361000, China., Zhang Y; School of Medicine, Xiamen University, Xiamen, 361000, China., Lu M; School of Medicine, Xiamen University, Xiamen, 361000, China., Zhao X; School of Medicine, Xiamen University, Xiamen, 361000, China., Wan Z; School of Medicine, Xiamen University, Xiamen, 361000, China. wanzheng0626@xmu.edu.cn. |
المصدر: | Nutrition & diabetes [Nutr Diabetes] 2024 Aug 06; Vol. 14 (1), pp. 60. Date of Electronic Publication: 2024 Aug 06. |
نوع المنشور: | Journal Article; Research Support, Non-U.S. Gov't |
اللغة: | English |
بيانات الدورية: | Publisher: Nature Pub. Group Country of Publication: England NLM ID: 101566341 Publication Model: Electronic Cited Medium: Internet ISSN: 2044-4052 (Electronic) Linking ISSN: 20444052 NLM ISO Abbreviation: Nutr Diabetes Subsets: MEDLINE |
أسماء مطبوعة: | Original Publication: Houndmills, Basingstoke : Nature Pub. Group, 2010- |
مواضيع طبية MeSH: | Non-alcoholic Fatty Liver Disease*/genetics , Non-alcoholic Fatty Liver Disease*/metabolism , Diabetes Mellitus, Type 2*/genetics , Diabetes Mellitus, Type 2*/metabolism , Computational Biology*/methods , Disease Models, Animal* , Protein Interaction Maps*, Animals ; Mice ; Kruppel-Like Factor 4 ; Male ; Mice, Inbred C57BL ; Gene Regulatory Networks ; Signal Transduction ; Gene Expression Profiling ; Humans |
مستخلص: | Background: Type 2 diabetes (T2D) and non-alcoholic fatty liver disease (NAFLD) are prevalent metabolic disorders with overlapping pathophysiological mechanisms. A comprehensive understanding of the shared molecular pathways involved in these conditions can advance the development of effective therapeutic interventions. Methods: We used two datasets sourced from the Gene Expression Omnibus (GEO) database to identify common differentially expressed genes (DEGs) between T2D and NAFLD. Subsequently, we conducted Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) analyses to identify the enriched biological processes and signaling pathways. In addition, we performed a protein-protein interaction (PPI) network analysis to identify hub genes with pivotal roles. To validate our findings, we established a type 2 diabetic mouse model with NAFLD. Results: Our analysis identified 53 DEGs shared between T2D and NAFLD. Enrichment analysis revealed their involvement in signal transduction, transcriptional regulation, and cell proliferation as well as in the ferroptosis signaling pathways. PPI network analysis identified ten hub genes, namely CD44, CASP3, FYN, KLF4, HNRNPM, HNRNPU, FUBP1, RUNX1, NOTCH3, and ANXA2. We validated the differential expression of FYN, HNRNPU, and FUBP1 in liver tissues of a type 2 diabetic mouse model with NAFLD. Conclusions: Our study offers valuable insights into the shared molecular mechanisms underlying T2D and NAFLD. The identified hub genes and pathways present promising prospects as therapeutic targets to address these prevalent metabolic disorders. (© 2024. The Author(s).) |
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معلومات مُعتمدة: | 2022J05298 Natural Science Foundation of Fujian Province (Fujian Provincial Natural Science Foundation); 2023J05049 Natural Science Foundation of Fujian Province (Fujian Provincial Natural Science Foundation); 82301227 National Natural Science Foundation of China (National Science Foundation of China) |
المشرفين على المادة: | 0 (Kruppel-Like Factor 4) 0 (Klf4 protein, mouse) |
تواريخ الأحداث: | Date Created: 20240806 Date Completed: 20240806 Latest Revision: 20240812 |
رمز التحديث: | 20240813 |
مُعرف محوري في PubMed: | PMC11303809 |
DOI: | 10.1038/s41387-024-00323-0 |
PMID: | 39107295 |
قاعدة البيانات: | MEDLINE |
تدمد: | 2044-4052 |
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DOI: | 10.1038/s41387-024-00323-0 |