ArticleOncotarget2016
MicroRNA-27a promotes renal tubulointerstitial fibrosis via suppressing PPARγ pathway in diabetic nephropathy.
Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers, 1 of them a synthesis 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.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
35 citing papers in PubMed, 1 synthesis or guideline pooled it, 60 citations in OpenAlex.
- Association between polymorphisms in microRNAs and susceptibility to diabetes mellitus: A meta-analysis.Medicine · 2019Pooled it
- Roles of the peroxisome proliferator-activated receptors (PPARs) in the pathogenesis of diabetic kidney disease (DKD).Cell death discovery · 2026Review
- Downregulation of miR-27a-3p Modulates TGF-β Signaling and Dysregulates Metabolism in Glioblastoma.International journal of molecular sciences · 2025Article
- Unveiling the Predictive Model for Macrovascular Complications in Type 2 Diabetes Mellitus: microRNAs Expression, Lipid Profile, and Oxidative Stress Markers.International journal of molecular sciences · 2024Article
- The Associations between Asprosine, Clusterin, Zinc Alpha-2-Glycoprotein, Nuclear Factor Kappa B, and Peroxisome Proliferator-Activated Receptor Gamma in the Development of Complications in Type 2 Diabetes Mellitus.Journal of clinical medicine · 2024Article
- Pulmonary Fibrosis and Diabetes Mellitus: Two coins with the same face.Archives of internal medicine research · 2024Article
- Isoflavone daidzein ameliorates renal dysfunction and fibrosis in a postmenopausal rat model: Intermediation of angiotensin AT1 and Mas receptors and microRNAs 33a and 27a.Iranian journal of basic medical sciences · 2022Article
- MicroRNAs in kidney injury and disease.Nature reviews. Nephrology · 2022Review
- Renal mitochondrial injury in the pathogenesis of CKD: mtDNA and mitomiRs.Clinical science (London, England : 1979) · 2022Review
- Druggability of lipid metabolism modulation against renal fibrosis.Acta pharmacologica Sinica · 2022Review
- PPARγ and TGFβ-Major Regulators of Metabolism, Inflammation, and Fibrosis in the Lungs and Kidneys.International journal of molecular sciences · 2021Review
- Downregulation of miR-17 suppresses TGF-β1-mediated renal fibrosis through targeting Smad7.Molecular and cellular biochemistry · 2021Article
- MicroRNA‑101 inhibits renal tubular epithelial‑to‑mesenchymal transition by targeting TGF‑β1 type I receptor.International journal of molecular medicine · 2021Article
- Article
- Pharmacokinetics and Proceedings in Clinical Application of Nucleic Acid Therapeutics.Molecular therapy : the journal of the American Society of Gene Therapy · 2021Review
- Protective mechanism of apigenin in diabetic nephropathy is related to its regulation of miR-423-5P-USF2 axis.American journal of translational research · 2021Article
- Construction and Bioinformatics Analysis of the miRNA-mRNA Regulatory Network in Diabetic Nephropathy.Journal of healthcare engineering · 2021Article
- Update on the Mechanisms of Tubular Cell Injury in Diabetic Kidney Disease.Frontiers in medicine · 2021Review
- Review
- Overexpression of Linc 4930556M19Rik Suppresses High Glucose-Triggered Podocyte Apoptosis, Fibrosis and Inflammation via the miR-27a-3p/Metalloproteinase 3 (TIMP3) Axis in Diabetic Nephropathy.Medical science monitor : international medical journal of experimental and clinical research · 2020Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
MicroRNA-27a (miR-27a) upregulation has been identified in diabetes, but the pathogenesis of miR-27a in renal tubulointerstitial fibrosis (TIF) in diabetic nephropathy (DN) has not been elucidated. Herein, we found that high glucose stimulated miR-27a expression, which directly inhibited PPARγ and promoted fibrosis in NRK-52E cells. The functional relevance of miR-27a-dependent PPARγ decrease was proven by inhibition or overexpression of miR-27a both in vitro and in streptozotocin-induced diabetic rats. MiR-27a, via repression of PPARγ, activates the TGF-β/Smad3 signaling and contributes to the expressional changes of connective tissue growth factor (CTGF), Fibronectin and Collagen I, key mediators of fibrosis. Furthermore, we provide evidences that plasma miR-27a upregulation contributed to unfavorable renal function and increased TIF in renal tissues of diabetic rats and DN patients. Notably, miR-27a exhibited clinical and biological relevance as it was linked to elevated serum creatinine, proteinuria, urinary N-acetyl-β-D-glucosaminidase (NAG), and reduced estimated glomerular filtration rate (eGFR). Thus, we propose a novel role of the miR-27a-PPARγ axis in fostering the progression toward more deteriorated renal TIF in DN. Monitoring plasma miR-27a level and its association with PPARγ can be used to reflect the severity of renal TIF. Targeting miR-27a could be evaluated as a potential therapeutic approach for DN.
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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 OpenQuestion graph.