ArticleMolecular therapy. Nucleic acids2019
lncRNA NR_038323 Suppresses Renal Fibrosis in Diabetic Nephropathy by Targeting the miR-324-3p/DUSP1 Axis.
Article in Molecular therapy. Nucleic acids, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 64 papers.
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Who cites it
64 citing papers in PubMed, 119 citations in OpenAlex.
- DUSP1 deficiency accelerates UVB‑induced HDF cell senescence by regulating ferroptosis.Photochemical & photobiological sciences : Official journal of the European Photochemistry Association and the European Society for Photobiology · 2026Article
- Upregulated CCN1 from pleural mesothelial cells alters collagen I conformation and drives fibrosis via ITGB1/MAPK signaling.Cellular & molecular biology letters · 2026Article
- Review
- Compound Analysis and Mechanistic Exploration of Shen-Yan-Fang-Shuai Formula in Diabetic Kidney Disease: An UHPLC-MS/MS and Bioinformatics Study.Journal of diabetes research · 2026Article
- Inflammation-related lncRNAs in the regulation of kidney injuries; special emphasis on novel lncRNA-based delivery platforms.Naunyn-Schmiedeberg's archives of pharmacology · 2026Review
- Deconvolution of molecular mechanisms in di-n-butyl phthalate/mono-n-butyl phthalate induced diabetic kidney disease by integrated machine learning and molecular docking.BMC nephrology · 2025Article
- Epidemiological and transcriptome data identify potential key genes involved in inflammatory response for diabetic nephropathy.Scientific reports · 2025Article
- LncRNA SNHG16 Drives PD-L1-Mediated Immune Escape in Colorectal Cancer through Regulating miR-324-3p/ELK4 Signaling.Biochemical genetics · 2025Article
- Bioinformatic analysis, clinical implications and experimental validation of ferroptosis-related feature gene in IgA nephropathy: focus on DUSP1.Frontiers in medicine · 2025Article
- Acetylation-regulated DUSP1 deficiency contributes to renal fibrosis progression.Theranostics · 2025Article
- Constructing the biomolecular networks associated with diabetic nephropathy and dissecting the effects of biomolecule variation underlying pathogenesis.Endocrine journal · 2024Article
- Long Non-coding RNA SNHG7 Suppresses Inflammation and Apoptosis of Chondrocytes Through Inactivating of p38 MAPK Signaling Pathway in Osteoarthritis.Molecular biotechnology · 2024Article
- The immune-inflammation factor is associated with diabetic nephropathy: evidence from NHANES 2013-2018 and GEO database.Scientific reports · 2024Article
- Research Progress of Pyroptosis in Diabetic Kidney Disease.International journal of molecular sciences · 2024Review
- Early growth response 1 regulates dual‑specificity protein phosphatase 1 and inhibits cell migration and invasion of tongue squamous cell carcinoma.Oncology letters · 2024Article
- N1F(Improved-Nephropathy 1 Formula) Ameliorates Renal Interstitial Fibrosis via Inhibiting Extracellular Matrix Deposition and Regulating the FGF23/P38MAPK/Wnt Pathway.Cell biochemistry and biophysics · 2024Article
- Chemical components in cultivatedChinese herbal medicines · 2024Article
- LncRNA HOX transcript antisense RNA mediates hyperglycemic-induced injury in the renal tubular epithelial cell via the miR-126-5pAkt axis.Aging medicine (Milton (N.S.W)) · 2023Article
- Ginsenoside Rg1 treatment alleviates renal fibrosis by inhibiting the NOX4-MAPK pathway in T2DM mice.Renal failure · 2023Article
- DUSP1 protects against ischemic acute kidney injury through stabilizing mtDNA via interaction with JNK.Cell death & disease · 2023Article
4 more citing papers are in PubMed but not listed here.
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Authors and funding
10 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Several studies have suggested that long intergenic noncoding RNAs are involved in the progression of diabetic nephropathy (DN). However, the exact role and regulatory mechanism of long noncoding RNA (lncRNA) NR_038323 in diabetic nephropathy (DN) remain largely unclear. In the present study, we found that lncRNA NR_038323 overexpression ameliorated the high glucose (HG)-induced expression levels of collagen I, collagen IV, and fibronectin, whereas lncRNA NR_038323 knockdown exerted the opposite effects. Moreover, the results of bioinformatic prediction, luciferase assay, and fluorescence in situ hybridization (FISH) demonstrated that lncRNA NR_038323 directly interacted with miR-324-3p. Additionally, miR-324-3p mimic aggravated the HG-induced expression levels of collagen I, collagen IV, and fibronectin by dual-specificity protein phosphatase-1 (DUSP1) expression to activate p38 mitogen-activated protein kinase (MAPK) and ERK1/2 pathways. In contrast, overexpression of DUSP1 attenuated the HG-induced expression levels of collagen I, collagen IV, and fibronectin via inactivation of p38 MAPK and ERK1/2 pathways. In addition, lncRNA NR_038323 knockdown increased the expression levels of collagen I, collagen IV, and fibronectin by upregulating DUSP1 expression during HG treatment, which were markedly reversed by miR-324-3p inhibitor. Furthermore, these molecular changes were verified in the human kidney samples of DN patients. Finally, overexpression of lncRNA NR_038323 ameliorated the interstitial fibrosis in STZ-induced diabetic nephrology (DN) rat via miR-324-3p/DUSP1/p38MAPK and ERK1/2 axis. In conclusion, our data indicate that overexpression of lncRNA NR_038323 may suppress HG-induced renal fibrosis via the miR-324-3p/DUSP1/p38MAPK and ERK1/2 axis, which provides new insights into the pathogenesis of DN.
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