ArticleJournal of the American Society of Nephrology : JASN2016
MicroRNA-23b Targets Ras GTPase-Activating Protein SH3 Domain-Binding Protein 2 to Alleviate Fibrosis and Albuminuria in Diabetic Nephropathy.
Article in Journal of the American Society of Nephrology : JASN, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 60 papers.
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Who cites it
60 citing papers in PubMed, 105 citations in OpenAlex.
- Review
- Research Progress on the Biological Function, Disease-Driving Mechanism and Clinical Targeting Strategies of G3BP2.Molecules (Basel, Switzerland) · 2026Review
- miRNAs in Glomerular Diseases: From Pathogenic Insight to Therapeutic Potential: A Narrative Review.Cells · 2026Review
- Review
- Identify the co-expressed genes of hypertensive nephropathy and diabetic nephropathy.Scientific reports · 2025Article
- Insights into non-coding RNAS: biogenesis, function and their potential regulatory roles in acute kidney disease and chronic kidney disease.Molecular and cellular biochemistry · 2025Review
- B-Cell Epigenetic Modulation of IgA Response by 5-Azacytidine and IgA Nephropathy.Journal of the American Society of Nephrology : JASN · 2024Article
- Urinary podocyte markers in diabetic kidney disease.Kidney research and clinical practice · 2024Article
- Identification of crosstalk genes relating to ECM-receptor interaction genes in MASH and DN using bioinformatics and machine learning.Journal of cellular and molecular medicine · 2024Article
- [Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2023Article
- Role(s) of G3BPs in Human Pathogenesis.The Journal of pharmacology and experimental therapeutics · 2023Review
- Article
- USP7- and PRMT5-dependent G3BP2 stabilization drives de novo lipogenesis and tumorigenesis of HNSC.Cell death & disease · 2023Article
- Ferroptosis: new insight into the mechanisms of diabetic nephropathy and retinopathy.Frontiers in endocrinology · 2023Review
- A Cyclopentanone Compound Attenuates the Over-Accumulation of Extracellular Matrix and Fibrosis in Diabetic Nephropathy via Downregulating the TGF-β/p38MAPK Axis.Biomedicines · 2022Article
- Nuclear paraspeckle assembly transcript 1 promotes the podocyte injury via targeting miR-23b-3p/B-cell lymphoma-2 interacting protein 3 like axis.Renal failure · 2022Article
- MicroRNAs in kidney injury and disease.Nature reviews. Nephrology · 2022Review
- KCNQ1OT1 inhibition alleviates high glucose-induced podocyte injury by adsorbing miR-23b-3p and regulating Sema3A.Clinical and experimental nephrology · 2022Article
- Targeting CC chemokine ligand (CCL) 20 by miR-143-5p alleviate lead poisoning-induced renal fibrosis by regulating interstitial fibroblasts excessive proliferation and dysfunction.Bioengineered · 2022Article
- Eight Differential miRNAs in DN Identified by Microarray Analysis as Novel Biomarkers.Diabetes, metabolic syndrome and obesity : targets and therapy · 2022Article
Corrections and comments
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Authors and funding
12 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Diabetic nephropathy (DN) is a frequent and severe complication of diabetes that is structurally characterized by glomerular basement membrane thickening, extracellular matrix accumulation, and destabilization of podocyte foot processes. MicroRNAs (miRNAs) are dysregulated in DN, but identification of the specific miRs involved remains incomplete. Here, we confirm that the peripheral blood from patients with diabetes and the kidneys of animals with type 1 or 2 diabetes have low levels of miR-23b compared with those of their nondiabetic counterparts. Furthermore, exposure to high glucose downregulated miR-23b in cultured kidney cells. In contrast, renal expression of Ras GTPase-activating protein SH3 domain-binding protein 2 (G3BP2), a putative miR-23b target, increased in DN. In vitro, overexpression of miR-23b decreased, and inhibition of miR-23b increased, G3BP2 expression levels. Bioinformatics analysis also revealed p53 binding sites in the miR-23b promoter; in vitro inhibition of p53 or the upstream p38 mitogen-activated protein kinase (p38MAPK) upregulated miR-23b expression in high-glucose conditions. In turn, inhibition of G3BP2 or overexpression of miR-23b downregulated p53 and p38MAPK expression in high-glucose conditions. In vivo, overexpression of miR-23b or inhibition of p53 in db/db mice reversed hyperalbuminuria and kidney fibrosis, whereas miR-23b antagomir treatment promoted renal fibrosis and increased albuminuria in wild-type mice. These data suggest that hyperglycemia regulates pathogenic processes in DN through an miR-23b/G3BP2 feedback circuit involving p38MAPK and p53. In conclusion, these results reveal a role for miR-23b in DN and indicate a novel potential therapeutic target.
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