ArticleJournal of cellular and molecular medicine2020
Loss of lncRNA MIAT ameliorates proliferation and fibrosis of diabetic nephropathy through reducing E2F3 expression.
Article in Journal of cellular and molecular medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers, 1 of them a synthesis that pooled it.
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Who cites it
18 citing papers in PubMed, 1 synthesis or guideline pooled it, 31 citations in OpenAlex.
- The Impact of lncRNA on Diabetic Kidney Disease: Systematic Review and In Silico Analyses.Computational intelligence and neuroscience · 2022Pooled it
- Inflammation-related lncRNAs in the regulation of kidney injuries; special emphasis on novel lncRNA-based delivery platforms.Naunyn-Schmiedeberg's archives of pharmacology · 2026Review
- Shared Genomic Features Between Lung Adenocarcinoma and Type 2 Diabetes: A Bioinformatics Study.Biology · 2025Article
- Influence of rsHealth science reports · 2025Article
- Mesangial Cells in Diabetic Kidney Disease: From Mechanisms to Therapeutic Implications.International journal of biological sciences · 2025Review
- AlteredExperimental biology and medicine (Maywood, N.J.) · 2025Article
- Nanopore-based full-length transcriptome sequencing for understanding the underlying molecular mechanisms of rapid and slow progression of diabetes nephropathy.BMC medical genomics · 2024Article
- Association between Genetic Polymorphism of The lncRNACell journal · 2023Article
- Renoprotective Potency of Sitagliptin versus Pioglitazone in Type 2 Diabetic Patients: Impact on LncMIAT.ACS omega · 2023Article
- microRNA-29b-3p attenuates diabetic nephropathy in mice by modifying EZH2.Hormones (Athens, Greece) · 2023Article
- Expression profiles of long non-coding RNAs in neurogenic bladder of spinal cord injured rats: a transcriptomic analysis.Translational andrology and urology · 2022Article
- LncRNA HOTAIR facilitates high glucose-induced mesangial cell proliferation, fibrosis and oxidative stress in diabetic nephropathy via regulating miR-147a/WNT2B axis.Diabetology & metabolic syndrome · 2022Article
- The role of lncRNAs in regulation of DKD and diabetes-related cancer.Frontiers in oncology · 2022Review
- LncRNAs regulate ferroptosis to affect diabetes and its complications.Frontiers in physiology · 2022Review
- Notoginsenoside R1 alleviates high glucose-induced inflammation and oxidative stress in HUVECs via upregulating miR-147a.The Kaohsiung journal of medical sciences · 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
- Long noncoding RNA MIAT inhibits the progression of diabetic nephropathy and the activation of NF-κB pathway in high glucose-treated renal tubular epithelial cells by the miR-182-5p/GPRC5A axis.Open medicine (Warsaw, Poland) · 2021Article
- Loss of lncRNA MIAT ameliorates proliferation and fibrosis of diabetic nephropathy through reducing E2F3 expression.Journal of cellular and molecular medicine · 2020Article
Corrections and comments
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Authors and funding
10 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Diabetic nephropathy (DN) is a serious kidney disease resulted from diabetes. Dys-regulated proliferation and extracellular matrix (ECM) accumulation in mesangial cells contribute to DN progression. In this study, we tested expression level of MIAT in DN patients and mesangial cells treated by high glucose (HG). Up-regulation of MIAT was observed in DN. Then, functional assays displayed that silence of MIAT by siRNA significantly repressed the proliferation and cycle progression in mesangial cells induced by HG. Meanwhile, we found that collagen IV, fibronectin and TGF-β1 protein expression was obviously triggered by HG, which could be rescued by loss of MIAT. Then, further assessment indicated that MIAT served as sponge harbouring miR-147a. Moreover, miR-147a was decreased in DN, which exhibited an antagonistic effect of MIAT on modulating mesangial cell proliferation and fibrosis. Moreover, bioinformatics analysis displayed that E2F transcription factor 3 (E2F3) could act as direct target of miR-147a. We demonstrated that E2F3 was greatly increased in DN and the direct binding association between miR-147a and E2F3 was evidenced using luciferase reporter assay. In summary, our data explored the underlying mechanism of DN pathogenesis validated that MIAT induced mesangial cell proliferation and fibrosis via sponging miR-147a and regulating E2F3.
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