ArticleScientific reports2023
Knockdown of lncRNA MALAT1 attenuates renal interstitial fibrosis through miR-124-3p/ITGB1 axis.
Article in Scientific reports, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 20 citations in OpenAlex.
- tRF-1-ArgTCG-1-1 promotes renal fibrosis by regulating β-catenin.Renal failure · 2026Article
- The versatile roles of long non-coding RNAs in kidney disease.Nature reviews. Nephrology · 2026Review
- Epitranscriptomics in kidney disease: insights and therapeutic potential.Kidney research and clinical practice · 2026Article
- JUNB transcriptional regulation of KRT20 via ITGB1 activates PI3K/AKT signaling pathway against fibrosis-induced by renal injury.Biology direct · 2026Article
- Review
- MicroRNA Regulation in Kidney Interstitial Fibrosis.Epigenomes · 2026Review
- Research progress on the interaction mechanisms and functions between exosomes and the cytoskeleton.Frontiers in cell and developmental biology · 2026Review
- Metformin alleviates the progression of oral submucous fibrosis through downregulation of metastasis associated lung adenocarcinoma transcript 1 (MALAT1).Journal of dental sciences · 2026Article
- Comprehensive analysis of pyroptosis-related gene signatures in renal fibrosis.Clinical and experimental nephrology · 2025Article
- Long non-coding RNA in IgA nephropathy: a comprehensive review.Renal failure · 2025Review
- Inflammation, Apoptosis, and Fibrosis in Diabetic Nephropathy: Molecular Crosstalk in Proximal Tubular Epithelial Cells and Therapeutic Implications.Current issues in molecular biology · 2025Review
- The NEAT1/miR-124-3p/CCL2 axis in chronic kidney disease progression: integrated bioinformatics analysis and experimental validation.Epigenomics · 2025Article
- Targeting long non-coding RNAMolecular therapy. Nucleic acids · 2025Article
- Long non-coding RNAMolecular therapy. Nucleic acids · 2025Review
- Immunological Features and Potential Biomarkers of Systemic Sclerosis-Associated Interstitial Lung Disease and Idiopathic Pulmonary Fibrosis.The clinical respiratory journal · 2025Article
- miR-124-3p inhibits CRC proliferation, migration, and invasion by targeting ITGB1.Discover oncology · 2025Article
- LncRNA MALAT1 Knockdown Alleviates Fibrogenic Response in Human Endometrial Stromal Cells Via the miR-22-3p/TGFβR1/Smad2/3 Pathway.Cell biochemistry and biophysics · 2024Article
- Research progress on miR-124-3p in the field of kidney disease.BMC nephrology · 2024Review
- Long noncoding RNA MALAT1 as a ceRNA drives mouse fibroblast activation via the miR-335-3p/P2ry2 axis.PloS one · 2024Article
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Authors and funding
9 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Renal interstitial fibrosis (RIF) considered the primary irreversible cause of chronic kidney disease. Recently, accumulating studies demonstrated that lncRNAs play an important role in the pathogenesis of RIF. However, the underlying exact mechanism of lncRNA MALAT1 in RIF remains barely known. Here, the aim of our study was to investigate the dysregulate expression of lncRNA MALAT1 in TGF-β1 treated HK2/NRK-49F cells and unilateral ureteral obstruction (UUO) mice model, defining its effects on HK2/NRK-49F cells and UUO mice fibrosis process through the miR-124-3p/ITGB1 signaling axis. It was found that lncRNA MALAT1 and ITGB1 was significantly overexpression, while miR-124-3p was downregulated in HK2/NRK-49F cells induced by TGF-β1 and in UUO mice model. Moreover, knockdown of lncRNA MALAT1 remarkably downregulated the proteins level of fibrosis-related markers, ITGB1, and upregulated the expression of epithelial marker E-cadherin. Consistently, mechanistic studies showed that miR-124-3p can directly binds to lncRNA MALAT1 and ITGB1. And the protect effect of Len-sh-MALAT1 on fibrosis related protein levels could be partially reversed by co-transfected with inhibitor-miR-124-3p. Moreover, the expression trend of LncRNA MALAT1/miR-124-3p/ITGB1 in renal tissues of patients with obstructive nephropathy (ON) was consistent with the results of cell and animal experiments. Taken together, these results indicated that lncRNA MALAT1 could promote RIF process in vitro and in vivo via the miR-124-3p/ITGB1 signaling pathway. These findings suggest a new regulatory pathway involving lncRNA MALAT1, which probably serves as a potential therapeutic target for RIF.
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