ArticleJournal of cellular and molecular medicine2017
LncRNA MALAT1 is dysregulated in diabetic nephropathy and involved in high glucose-induced podocyte injury via its interplay with β-catenin.
Article in Journal of cellular and molecular medicine, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 124 papers, 2 of them syntheses that pooled it.
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Who cites it
124 citing papers in PubMed, 2 syntheses or guidelines pooled it, 194 citations in OpenAlex.
- Focus on podocytes: diabetic kidney disease and renal fibrosis - a global bibliometric analysis (2000-2024).Frontiers in pharmacology · 2024Pooled it
- The Impact of lncRNA on Diabetic Kidney Disease: Systematic Review and In Silico Analyses.Computational intelligence and neuroscience · 2022Pooled it
- Prevalence of Inflammatory Pathways Over Immuno-Tolerance in Peripheral Blood Mononuclear Cells of Recent-Onset Type 1 Diabetes.Frontiers in immunology · 2021Trial
- LncRNA Gm44981 modulates EZH2-H3K27me3-p21 axis to suppress mesangial cell senescence and kidney aging.Renal failure · 2026Article
- In silico analysis of MALAT1 and H19 lncRNA interactions with the diabetes-related proteins ASK1 and YAP1.In silico pharmacology · 2026Article
- Associations of MALAT1 rs619586/rs3200401 and ANRIL rs10965215/rs10738605 polymorphisms with type 2 diabetes and diabetic nephropathy risk in an Egyptian population.Frontiers in endocrinology · 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
- METTL3 promotes podocyte pyroptosis in diabetic nephropathy through NRenal failure · 2025Article
- Review
- Article
- LncRNA ENST00000532153.1 alleviates podocyte injury by inhibiting PARP1-mediated PARylation of ATF3 in diabetic kidney disease.Cellular and molecular life sciences : CMLS · 2025Article
- Targeting long non-coding RNAMolecular therapy. Nucleic acids · 2025Article
- METTL3-Mediated N6-Methyladenosine Modification Regulates the Progression of Diabetic Retinopathy.Applied biochemistry and biotechnology · 2025Article
- Mitochondrial Fragmentation and Long Noncoding RNAInternational journal of molecular sciences · 2025Article
- Cellular and Molecular Resolution of Focal Segmental Glomerulosclerosis Recurrence in Human Allografts.bioRxiv : the preprint server for biology · 2025Article
- Advances in focal segmental glomerulosclerosis research: genetic causes to non-coding RNAs.Molecular biology reports · 2025Review
- Stress-Related LncRNAs and Their Roles in Diabetes and Diabetic Complications.International journal of molecular sciences · 2025Review
- Regulation of energy metabolism by non-coding RNAs in livestock species: a review.Journal of comparative physiology. B, Biochemical, systemic, and environmental physiology · 2025Review
- Understanding the Roles of Non-coding RNAs and Exosomal Non-Coding RNAs in Diabetic Nephropathy.Current molecular medicine · 2025Review
- LPItabformer: Enhancing generalization in predicting lncRNA-protein interactions via a tabular Transformer.Computational and structural biotechnology journal · 2025Article
64 more citing papers are in PubMed but not listed here.
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Authors and funding
8 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Metastasis associated lung adenocarcinoma transcript 1(MALAT1) is a long non-coding RNA, broadly expressed in mammalian tissues including kidney and up-regulated in a variety of cancer cells. To date, its functions in podocytes are largely unknown. β-catenin is a key mediator in the canonical and non-canonical Wnt signalling pathway; its aberrant expression promotes podocyte malfunction and albuminuria, and contributes to kidney fibrosis. In this study, we found that MALAT1 levels were increased in kidney cortices from C57BL/6 mice with streptozocin (STZ)-induced diabetic nephropathy, and dynamically regulated in cultured mouse podocytes stimulated with high glucose, which showed a trend from rise to decline. The decline of MALAT1 levels was accompanied with β-catenin translocation to the nuclei and enhanced expression of serine/arginine splicing factor 1 (SRSF1), a MALAT1 RNA-binding protein. Further we showed early interference with MALAT1 siRNA partially restored podocytes function and prohibited β-catenin nuclear accumulation and SRSF1 overexpression. Intriguingly, we showed that β-catenin was involved in MALAT1 transcription by binding to the promotor region of MALAT1; β-catenin knock-down also decreased MALAT1 levels, suggesting a novel feedback regulation between MALAT1 and β-catenin. Notably, β-catenin deletion had limited effects on SRSF1 expression, demonstrating β-catenin might serve as a downstream signal of SRSF1. These findings provided evidence for a pivotal role of MALAT1 in diabetic nephropathy and high glucose-induced podocyte damage.
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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.