ArticlePeerJ2019
Long noncoding RNA MEG3 suppresses podocyte injury in diabetic nephropathy by inactivating Wnt/β-catenin signaling.
Article in PeerJ, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 23 citations in OpenAlex.
- Correlation of differential expression of MEG3 lnc-RNA with biochemical parameters in Type-II diabetic patients with and without diabetic kidney disease.Pakistan journal of medical sciences · 2026Article
- Long noncoding RNA MEG3: an active player in fibrosis.Pharmacological reports : PR · 2025Review
- Investigating circulating expression profile forFrontiers in molecular biosciences · 2025Article
- Non-coding RNAs as therapeutic targets in cancer and its clinical application.Journal of pharmaceutical analysis · 2024Review
- LncRNA MEG3 inhibits renal fibrinoid necrosis of diabetic nephropathy via the MEG3/miR-21/ORAI1 axis.Molecular biology reports · 2023Article
- Exploring the mechanisms underlying the therapeutic effect of the drug pair Rhubarb-Coptis in diabetic nephropathy using network pharmacology and molecular docking analysis.Annals of translational medicine · 2022Article
- Long Noncoding RNA MEG3-205/Let-7a/MyD88 Axis Promotes Renal Inflammation and Fibrosis in Diabetic Nephropathy.Kidney diseases (Basel, Switzerland) · 2022Article
- Regulation of Oxidative Stress by Long Non-Coding RNAs in Vascular Complications of Diabetes.Life (Basel, Switzerland) · 2022Review
- The role of lncRNAs in regulation of DKD and diabetes-related cancer.Frontiers in oncology · 2022Review
- Long non-coding RNAs in metabolic disorders: pathogenetic relevance and potential biomarkers and therapeutic targets.Journal of endocrinological investigation · 2021Review
- Placental maternally expressed gene 3 differentially methylated region methylation profile is associated with maternal glucose concentration and newborn birthweight.Journal of diabetes investigation · 2021Article
- Article
- 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
- Gene Transcript Alterations in the Spinal Cord, Anterior Cingulate Cortex, and Amygdala in Mice Following Peripheral Nerve Injury.Frontiers in cell and developmental biology · 2021Article
- Absence of Long Noncoding RNA H19 Promotes Childhood Nephrotic Syndrome through Inhibiting ADCK4 Signal.Medical science monitor : international medical journal of experimental and clinical research · 2020Article
Corrections and comments
- Expression of concern · 2024-11-24Concerns/Issues about Image · Investigation by Journal/Publisher · Updated to Retraction · · See also: https://pubpeer.com/publications/2281886EB39E6CA357E328E1EB45CF#0
- Retraction · 2025-10-10Concerns/Issues about Image · Investigation by Journal/Publisher · Investigation by Third Party · Lack of IRB/IACUC Approval and/or Compliance · Upgrade/Update of Prior Notice(s) · · See also: https://pubpeer.com/publications/2281886EB39E6CA357E328E1EB45CF#0
Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundDiabetic nephropathy (DN) is one of the principal complications of diabetes and podocyte injury plays an important role in the DN pathogenesis. Wnt/β-catenin signaling overactivation confers podocyte injury and promotes multiple types of renal disease. However, the underlying mechanism of Wnt/β-catenin signaling activation in DN progression has not been fully elucidated. Long noncoding RNA (lncRNA) is a large class of endogenous RNA molecules lacking functional code capacity and which participates in the pathogenesis of human disease, including DN.
methodA diabetes model was constructed by intraperitoneal injection of Streptozotocin in rats. The MPC5 cells were used to create the in vitro model. Western blot and Quantitative reverse-transcriptase-PCR were used to examine the expression of protein and mRNA. The migrated capacity was analyzed by Transwell migration assay. The cell viability was detected by CCK8.
resultsIn the present study, we revealed the association of lncRNA Maternally Expressed Gene 3 (MEG3) with aberrant activation of Wnt/β-catenin signaling and the role of MEG3/Wnt axis in podocyte injury. We found that high glucose (HG) treatment suppressed MEG3 expression in cultured podocytes, activated Wnt/β-catenin signaling and caused podocyte injury as indicated by the downregulation of podocyte-specific markers (podocin and synaptopodin) and the upregulation of snail1 and α-smooth muscle actin. Overexpression of MEG3 attenuated HG-induced podocyte injury by reducing Wnt/β-catenin activity, repressing cell migration, reactive oxygen species production and increasing the viability of podocytes. Furthermore, we provided evidences that restoration of Wnt/β-catenin signaling by specific agonist impeded the protective effect of MEG3 on podocyte injury. Current results demonstrated that MEG3/Wnt axis plays an important role in fostering podocyte injury and may serve as a potential therapeutic target for the treatment of DN.
conclusionlncRNA MEG3 ameliorates podocyte injury in DN via inactivating Wnt/β-catenin signaling.
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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.