ArticleBMC nephrology2014
Involvement of inflammation-related miR-155 and miR-146a in diabetic nephropathy: implications for glomerular endothelial injury.
Article in BMC nephrology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 85 papers, 2 of them syntheses that pooled it.
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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
85 citing papers in PubMed, 2 syntheses or guidelines pooled it, 147 citations in OpenAlex.
- A systematic review of urinary extracellular vesicle-derived non-coding RNAs in diabetic nephropathy: expression profiles, clinical correlations, and diagnostic performance.Molecular biology reports · 2026Pooled it
- Identification of candidate microRNA biomarkers in diabetic nephropathy: a meta-analysis of profiling studies.Journal of nephrology · 2018Pooled it
- Review
- miRNA in the Progression of Diabetic Kidney Disease: New Insight.International journal of molecular sciences · 2025Review
- Selected miRNAs in Urinary Extracellular Vesicles Show Promise for Early and Specific Diagnostics of Diabetic Kidney Disease.Journal of extracellular biology · 2025Article
- High Glucose Promotes the Ferroptosis and Dysfunction of Endothelial Cells by Downregulating SLC3A2 and Promoting the Development of Nephropathy.International journal of endocrinology · 2025Article
- Diabetes mellitus-driven pulmonary injury: multidimensional mechanisms linking metabolic dysregulation to gut-lung axis and promising therapies.Frontiers in pharmacology · 2025Review
- Astaxanthin Modulates Inflammation in Type 2 Diabetes via Regulation of microRNAs, Lysophosphatidylcholine, and α-Hydroxybutyrate.International journal of endocrinology · 2025Article
- MiR-146a participates in regulating the progression of periodontitis through the Wnt/β-catenin signaling pathway.PloS one · 2025Article
- A Systematic Review and Meta-Analysis of microRNA Profiling Studies in Chronic Kidney Diseases.Non-coding RNA · 2024Review
- Review
- microRNA Expression Profile in Obesity-Induced Kidney Disease Driven by High-Fat Diet in Mice.Nutrients · 2024Article
- Association between erythrocyte membrane fatty acids and gut bacteria in obesity-related cognitive dysfunction.AMB Express · 2023Article
- A mutual regulatory loop between miR-155 and SOCS1 influences renal inflammation and diabetic kidney disease.Molecular therapy. Nucleic acids · 2023Article
- MicroRNA193a: An Emerging Mediator of Glomerular Diseases.Biomolecules · 2023Review
- Article
- Epigenetics in Obesity and Diabetes Mellitus: New Insights.Nutrients · 2023Review
- miR-372-3p is a potential diagnostic factor for diabetic nephropathy and modulates high glucose-induced glomerular endothelial cell dysfunction via targeting fibroblast growth factor-16.Archives of medical science : AMS · 2023Article
- Association of MicroRNA-146a with Type 1 and 2 Diabetes and their Related Complications.Journal of diabetes research · 2023Review
- Article
25 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
14 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundMicroRNAs have been demonstrated to play an important role in the pathogenesis of diabetic nephropathy (DN). In this study, we investigated both the repertoire of miRNAs in the kidneys of patients with DN and their potential regulatory role in inflammation-mediated glomerular endothelial injury.
methodsThe miRNA expression profiling of the renal biopsy samples was performed by a microarray analysis; then, in situ hybridization and real-time polymerase chain reaction (PCR) were used to determine the localization and expression of two of the miRNAs significantly up-regulated in human DN kidney samples, miR-155 and miR-146a, in the kidney tissues from type 1 and type 2 DN rat models. Human renal glomerular endothelial cells (HRGECs) cultured under high-glucose conditions were transfected with miR-155 and miR-146a mimics, and the transforming growth factor (TGF)-β1, tumor necrosis factor (TNF)-α, and nuclear factor (NF)-κB expressions were examined by western blot, real-time PCR, and an electrophoresis mobility shift assay.
resultsThe expression of both miR-155 and miR-146a was increased more than fivefold in the kidney samples of the DN patients compared with the controls, and the miR-155 expression was closely correlated with the serum creatinine levels (R = 0.95, P = 0.004). During the induction and progression of the disease in type 1 and type 2 DN rat models, miR-155 and miR-146a were demonstrated to increase gradually. In vitro, high glucose induced the over-expression of miR-155 and miR-146a in the HRGECs, which, in turn, increased the TNF-α, TGF-β1, and NF-κB expression.
conclusionsTaken together, these findings indicate that the increased expression of miR-155 and miR-146a in the DN patients and in the experimental DN animal models was found to contribute to inflammation-mediated glomerular endothelial injury.
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