ArticleInternational journal of clinical and experimental pathology2019
LncRNA TUG1 ameliorates diabetic nephropathy by inhibiting miR-21 to promote TIMP3-expression.
Article in International journal of clinical and experimental pathology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 30 citations in OpenAlex.
- LncRNA RAD51-AS1 Alleviates Oxidative Stress and Inflammation in Diabetic Nephropathy by Adsorbing miR-154-5p.Kidney & blood pressure research · 2026Article
- METTL3 alleviates renal tubular mitochondrial dysfunction by regulating the TUG1/PGC-1a axis in an IGF2BP2-dependent manner in diabetic nephropathy.Renal failure · 2025Article
- lncRNA TUG1 and kidney diseases.BMC nephrology · 2025Review
- Uncovering the Mechanisms of Cinnamic Acid Treating Diabetic Nephropathy based on Network Pharmacology, Molecular Docking, and Experimental Validation.Current computer-aided drug design · 2025Article
- Urinary podocyte markers in diabetic kidney disease.Kidney research and clinical practice · 2024Article
- Diabetes and diabetic associative diseases: An overview of epigenetic regulations of TUG1.Saudi journal of biological sciences · 2024Review
- LncRNAs in oncogenic microenvironment: from threat to therapy.Frontiers in cell and developmental biology · 2024Review
- LncRNA TUG1 promotes pulmonary fibrosis progression via up-regulating CDC27 and activating PI3K/Akt/mTOR pathway.Epigenetics · 2023Article
- METTL14 promotes the development of diabetic kidney disease by regulating mActa diabetologica · 2023Article
- Long non-coding RNAs TUG1 and MEG3 in patients with type 2 diabetes and their association with endoplasmic reticulum stress markers.Journal of endocrinological investigation · 2023Article
- LncRNA NEAT2 Modulates Pyroptosis of Renal Tubular Cells Induced by High Glucose in Diabetic Nephropathy (DN) by via miR-206 Regulation.Biochemical genetics · 2022Article
- MicroRNA-21: A Critical Pathogenic Factor of Diabetic Nephropathy.Frontiers in endocrinology · 2022Review
- Expression of LncRNA KCNQ1Ot1 in diabetic nephropathy and its correlation with MEK/ERK signaling pathway.American journal of translational research · 2022Article
- The role of lncRNAs in regulation of DKD and diabetes-related cancer.Frontiers in oncology · 2022Review
- Long non-cording RNA XIST promoted cell proliferation and suppressed apoptosis by miR-423-5p/HMGA2 axis in diabetic nephropathy.Molecular and cellular biochemistry · 2021Article
- TIMP3 involvement and potentiality in the diagnosis, prognosis and treatment of diabetic nephropathy.Acta diabetologica · 2021Review
- LncRNA TUG1 attenuates ischaemia-reperfusion-induced apoptosis of renal tubular epithelial cells by sponging miR-144-3p via targeting Nrf2.Journal of cellular and molecular medicine · 2021Article
- Long non-coding RNA CASC2 restrains high glucose-induced proliferation, inflammation and fibrosis in human glomerular mesangial cells through mediating miR-135a-5p/TIMP3 axis and JNK signaling.Diabetology & metabolic syndrome · 2021Article
- LncRNA TUG1 exhibits pro-fibrosis activity in hypertrophic scar through TAK1/YAP/TAZ pathway via miR-27b-3p.Molecular and cellular biochemistry · 2021Article
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Diabetic nephropathy (DN) is one of the most important microvascular diseases in diabetic patients and has been the first cause of end stage renal disease (ESRD). In this study, we are aims to investigate the genetic mechanisms of lncRNA in the regulation of DN renal fibrosis. First, we have found that the expression of lncRNA TUG1 in db/db DN mice kidney tissue and high glucose-stimulated NRK-52E cells were down-regulated and the overexpression of lncRNA TUG1 could inhibit cell fibrosis of high glucose-stimulated of NRK-52E. Second, online software program Starbase predicts that miR-21 is a target gene of lncRNA TUG1 and TIMP3 is the target gene of miR-21, which have been verified by luciferase reporter assay and RNA Binding Protein Immunoprecipitation (RIP). Last, the renal fibrosis in DN mice and cell fibrosis in high glucose-stimulated NRK-52E cells were also evaluated. We have proven that overexpression of lncRNA TUG1 can promote the expression of TIMP3 through targeting the miR-21, thereby inhibiting cell fibrosis in high glucose-stimulated NRK-52E cells and renal fibrosis in DN mice. Our results indicated that lncRNA TUG1 could indirectly regulated the expression of TIMP3 by targeting miR-21. LncRNA TUG1 inhibited high glucose-stimulated NRK-52E cell fibrosis and renal fibrosis in DN mice, which provides a theoretical basis for the treatment of DN fibrosis.
Indexed as
Identifiers
31933879PMC6945187W3008786021What OpenQuestion holds
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.