ArticleHuman cell2018
Down-regulation of miR-23a inhibits high glucose-induced EMT and renal fibrogenesis by up-regulation of SnoN.
Article in Human cell, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers, 1 of them a synthesis that pooled it.
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Who cites it
26 citing papers in PubMed, 1 synthesis or guideline pooled it, 41 citations in OpenAlex.
- Identification of candidate microRNA biomarkers in diabetic nephropathy: a meta-analysis of profiling studies.Journal of nephrology · 2018Pooled it
- MicroRNA Regulation in Kidney Interstitial Fibrosis.Epigenomes · 2026Review
- Clinical Importance of miRNA in Diabetic Neuropathy: Pathophysiology, Diagnosis, and Therapeutic Potential.Current diabetes reviews · 2026Review
- Circulating microRNAs miR-21-5p, miR-23a-3p and miR-26a-5p reflect clinical and molecular features of aging.Scientific reports · 2025Article
- LP340, a novel histone deacetylase inhibitor, decreases liver injury and fibrosis in mice: role of oxidative stress and microRNA-23a.Frontiers in pharmacology · 2024Article
- Article
- The Role of miRNA in Renal Fibrosis Leading to Chronic Kidney Disease.Biomedicines · 2023Review
- Article
- Epigenetics of the Pathogenesis and Complications of Type 2 Diabetes Mellitus.TouchREVIEWS in endocrinology · 2023Review
- SKI knockdown suppresses apoptosis and extracellular matrix degradation of nucleus pulposus cells via inhibition of the Wnt/β-catenin pathway and ameliorates disc degeneration.Apoptosis : an international journal on programmed cell death · 2022Article
- Urinary microRNAome in healthy cats and cats with pyelonephritis or other urological conditions.PloS one · 2022Article
- Recent Advances in Diabetic Kidney Diseases: From Kidney Injury to Kidney Fibrosis.International journal of molecular sciences · 2021Review
- A transcription factor DAF-5 functions in Haemonchus contortus development.Parasites & vectors · 2021Article
- Urinary exosomal microRNA profiling in type 2 diabetes patients taking dipeptidyl peptidase-4 inhibitor compared with sulfonylurea.Kidney research and clinical practice · 2021Article
- Urinary Extracellular Vesicles and Their miRNA Cargo in Patients with Fabry Nephropathy.Genes · 2021Article
- Effects of metabolic memory on inflammation and fibrosis associated with diabetic kidney disease: an epigenetic perspective.Clinical epigenetics · 2021Review
- The Ubiquitin Proteasome System and Skin Fibrosis.Molecular diagnosis & therapy · 2021Review
- Update on the Mechanisms of Tubular Cell Injury in Diabetic Kidney Disease.Frontiers in medicine · 2021Review
- Intratumoral Fibrosis in Facilitating Renal Cancer Aggressiveness: Underlying Mechanisms and Promising Targets.Frontiers in cell and developmental biology · 2021Review
- Immunomodulatory and Regenerative Effects of Mesenchymal Stem Cell-Derived Extracellular Vesicles in Renal Diseases.International journal of molecular sciences · 2020Review
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
It has been reported that transforming growth factor-β1 (TGF-β1) signaling plays an important role in the development of diabetic nephropathy (DN). The nuclear transcription co-repressor Ski-related novel protein N (SnoN) is a critical negative regulator of TGF-β1/Smad signal pathway, involving in tubule epithelial-mesenchymal transition (EMT), extracellular matrix (ECM) accumulation, and tubulointerstitial fibrosis. In this study, we focused on miR-23a as a regulator of SnoN. Our purpose is to study the effects of miR-23a on high glucose (HG)-induced EMT process and ECM deposition in HK2 cells. We found that miR-23a was up-regulated in renal tissues of diabetic patients and HG-induced HK2 cells. Besides, the high level of miR-23a was closely associated with decreased SnoN expression. Knockdown of miR-23a increased SnoN expression and in turn suppressed HG-induced EMT and renal fibrogenesis. Introduction of miR-23a decreased SnoN expression and enhanced the profibrogenic effects of HG on HK2 cells. Next, bioinformatics analysis predicted that the SnoN was a potential target gene of miR-23a. Luciferase reporter assay demonstrated that miR-23a could directly target SnoN. We demonstrated that overexpression of SnoN was sufficient to inhibit HG-induced EMT and renal fibrogenesis in HK2 cells. Furthermore, down-regulation of SnoN partially reversed the protective effect of miR-23a knockdown on HG-induced EMT and renal fibrogenesis in HK2 cells. Collectively, miR-23a and SnoN significantly impact on the progression of HG-induced EMT and renal fibrogenesis in vitro, and they may represent novel targets for the prevention strategies of renal fibrosis in the context of DN.
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