ArticleThe Journal of biological chemistry2011
MicroRNA-21 orchestrates high glucose-induced signals to TOR complex 1, resulting in renal cell pathology in diabetes.
Article in The Journal of biological chemistry, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 131 papers, 1 of them a synthesis that pooled it.
What it found
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The trial behind it
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
131 citing papers in PubMed, 1 synthesis or guideline pooled it, 227 citations in OpenAlex.
- Identification of candidate microRNA biomarkers in diabetic nephropathy: a meta-analysis of profiling studies.Journal of nephrology · 2018Pooled it
- MicroRNA-21 in glomerular injury.Journal of the American Society of Nephrology : JASN · 2015Trial
- Kinase regulation of miRNA networks in cardiometabolic disease: emerging pathways to precision therapy.Journal of molecular medicine (Berlin, Germany) · 2026Review
- The UBR5 protein facilitates mesangial cell hypertrophy and glycolysis induced by high glucose by increasing the phosphorylation levels of AKT.Acta diabetologica · 2025Article
- Therapeutic Applications of Poly-miRNAs and miRNA Sponges.International journal of molecular sciences · 2025Review
- High glucose couples DJ-1 with PTEN to activate PDGFRβ for renal proximal tubular cell injury.PloS one · 2025Article
- Understanding the Roles of Non-coding RNAs and Exosomal Non-Coding RNAs in Diabetic Nephropathy.Current molecular medicine · 2025Review
- Dysfunction of PTEN-Associated MicroRNA Regulation: Exploring Potential Pathological Links in Type 1 Diabetes Mellitus.Medicina (Kaunas, Lithuania) · 2024Article
- New insights on genetic background of major diabetic vascular complications.Diabetology & metabolic syndrome · 2024Article
- Molecular Therapeutics for Diabetic Kidney Disease: An Update.International journal of molecular sciences · 2024Review
- Effects of HIIT training and HIIT combined with circuit resistance training on measures of physical fitness, miRNA expression, and metabolic risk factors in overweight/obese middle-aged women.BMC sports science, medicine & rehabilitation · 2024Article
- Rephrasing the 'David-Goliath' story in the field of diabetes.Molecular biology reports · 2024Review
- Influence of Different Glucose Concentrations on the Expression of miR-29c-3p microRNA in Mesenchymal Stem Cells.International journal of hematology-oncology and stem cell research · 2024Article
- Decoding the secrets of longevity: unraveling nutraceutical and miRNA-Mediated aging pathways and therapeutic strategies.Frontiers in aging · 2024Review
- The relevance of the non-invasive biomarkers lncRNA GAS5/miR-21 ceRNA regulatory network in the early identification of diabetes and diabetic nephropathy.Diabetology & metabolic syndrome · 2023Article
- MicroRNA-21 Silencing in Diabetic Nephropathy: Insights on Therapeutic Strategies.Biomedicines · 2023Review
- Article
- The Role of MicroRNA in the Pathogenesis of Diabetic Nephropathy.International journal of molecular sciences · 2023Review
- Effect of Selenium Nanoparticles and/or Bee Venom against STZ-Induced Diabetic Cardiomyopathy and Nephropathy.Metabolites · 2023Article
- Pediatric Diabetic Nephropathy: Novel Insights from microRNAs.Journal of clinical medicine · 2023Article
71 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
Hyperglycemia induces a wide array of signaling pathways in the kidney that lead to hypertrophy and matrix expansion, eventually culminating in progressive kidney failure. High glucose-induced reduction of the tumor suppressor protein phosphatase and tensin homolog deleted in chromosome 10 (PTEN) contributes to renal cell hypertrophy and matrix expansion. We identified microRNA-21 (miR-21) as the molecular link between high glucose and PTEN suppression. Renal cortices from OVE26 type 1 diabetic mice showed significantly elevated levels of miR-21 associated with reduced PTEN and increased fibronectin content. In renal mesangial cells, high glucose increased the expression of miR-21, which targeted the 3'-UTR of PTEN mRNA to inhibit PTEN protein expression. Overexpression of miR-21 mimicked the action of high glucose, which included a reduction in PTEN expression and a concomitant increase in Akt phosphorylation. In contrast, expression of miR-21 Sponge, to inhibit endogenous miR-21, prevented down-regulation of PTEN and phosphorylation of Akt induced by high glucose. Interestingly, high glucose-stimulated miR-21 inactivated PRAS40, a negative regulator of TORC1. Finally, miR-21 enhanced high glucose-induced TORC1 activity, resulting in renal cell hypertrophy and fibronectin expression. Thus, our results identify a previously unrecognized function of miR-21 that is the reciprocal regulation of PTEN levels and Akt/TORC1 activity that mediate critical pathologic features of diabetic kidney disease.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.