ArticleJournal of physiology and biochemistry2019
lncRNA MALAT1 mediated high glucose-induced HK-2 cell epithelial-to-mesenchymal transition and injury.
Article in Journal of physiology and biochemistry, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed, 50 citations in OpenAlex.
- Metabolic Memory-Mediated Epigenetic Regulation of EMT in Diabetic Kidney Disease: Mechanisms and Therapeutic Implications.International journal of molecular sciences · 2026Review
- In silico analysis of MALAT1 and H19 lncRNA interactions with the diabetes-related proteins ASK1 and YAP1.In silico pharmacology · 2026Article
- Stress-Related LncRNAs and Their Roles in Diabetes and Diabetic Complications.International journal of molecular sciences · 2025Review
- Constructing the biomolecular networks associated with diabetic nephropathy and dissecting the effects of biomolecule variation underlying pathogenesis.Endocrine journal · 2024Article
- LncRNA as a regulator in the development of diabetic complications.Frontiers in endocrinology · 2024Review
- Targeting lncRNA MALAT1: A Promising Approach to Overcome Metabolic Syndrome.International journal of endocrinology · 2024Review
- METTL14 promotes the development of diabetic kidney disease by regulating mActa diabetologica · 2023Article
- Astragalus polysaccharide promotes autophagy and alleviates diabetic nephropathy by targeting the lncRNA Gm41268/PRLR pathway.Renal failure · 2023Article
- High glucose induces an activated state of partial epithelial-mesenchymal transition in human primary tubular cell cultures.PloS one · 2023Article
- LINC02381, a sponge of miR-21, weakens osteogenic differentiation of hUC-MSCs through KLF12-mediated Wnt4 transcriptional repression.Journal of bone and mineral metabolism · 2022Article
- Long Non-Coding RNAs in the Pathogenesis of Diabetic Kidney Disease.Frontiers in cell and developmental biology · 2022Review
- LncRNA MALAT1 Aggravates Renal Tubular InjuryFrontiers in endocrinology · 2022Article
- lncRNA MALAT1 Promotes Diabetic Nephropathy Progression via miR-15b-5p/TLR4 Signaling Axis.Journal of immunology research · 2022Article
- Blocking REDD1/TXNIP Complex Ameliorates HG-Induced Renal Tubular Epithelial Cell Apoptosis and EMT through Repressing Oxidative Stress.International journal of endocrinology · 2022Article
- An integrated RNA sequencing and network pharmacology approach reveals the molecular mechanism of dapagliflozin in the treatment of diabetic nephropathy.Frontiers in endocrinology · 2022Article
- LncRNAs regulate ferroptosis to affect diabetes and its complications.Frontiers in physiology · 2022Review
- The role of lncRNAs in regulation of DKD and diabetes-related cancer.Frontiers in oncology · 2022Review
- CDKN2B-AS1 participates in high glucose-induced apoptosis and fibrosis via NOTCH2 through functioning as a miR-98-5p decoy in human podocytes and renal tubular cells.Diabetology & metabolic syndrome · 2021Article
- lncRNA‑MALAT1 promotes high glucose‑induced H9C2 cardiomyocyte pyroptosis by downregulating miR‑141‑3p expression.Molecular medicine reports · 2021Article
- LncRNA PVT1 Regulates High Glucose-Induced Viability, Oxidative Stress, Fibrosis, and Inflammation in Diabetic Nephropathy via miR-325-3p/Snail1 Axis.Diabetes, metabolic syndrome and obesity : targets and therapy · 2021Article
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Authors and funding
10 authors at 6 institutions in 2 countries.
Funding
Abstract
Epithelial-to-mesenchymal transition (EMT) and injury of tubular cells play critical roles in the pathogenesis of diabetic nephropathy (DN). lncRNA metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) has been shown to be involved in DN progression. However, whether MALAT1 induces EMT and injury in tubular cells is unclear. Here, we investigated the effects of MALAT1 on human proximal tubular cells (HK-2 cells) and the underlying mechanism. We performed qPCR to detect MALAT1, E-cadherin, α-smooth muscle actin (α-SMA), kidney injury molecule 1 (KIM-1), and neutrophil gelatinase-associated lipocalin (NGAL). Additionally, we conducted Western blot analyses to measure E-cadherin, α-SMA, cyclin D1, c-Myc, and β-catenin in HK-2 cells cultured with normal glucose and high glucose (HG) and in transfected cells or cells treated with LiCl and DKK-1. The β-catenin localization was observed using immunofluorescence, and the protein levels of NGAL and KIM-1 were evaluated by ELISA. We found that HG-upregulated MALAT1 decreased E-cadherin and increased α-SMA, KIM-1, NGAL, cyclin D1, c-Myc, and β-catenin in HK-2 cells. LiCl exposure increased the expression of α-SMA but decreased that of E-cadherin on the base of knocking down MALAT1, and decreased NGAL and KIM-1 expression. DKK-1 showed the opposite effects. Our results suggested that upregulated MALAT1 induced EMT in HG-treated HK-2 cells through activating the Wnt/β-catenin pathway. However, MALAT1-mediated injury in HK-2 cells was not mediated by activation of the Wnt/β-catenin pathway. Our results indicate that MALAT1 might serve as a novel therapeutic target for suppressing the progression of DN.
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