ArticleScientific reports2018
MALAT1: An Epigenetic Regulator of Inflammation in Diabetic Retinopathy.
Article in Scientific reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 85 papers, 1 of them a synthesis that pooled it.
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Who cites it
85 citing papers in PubMed, 1 synthesis or guideline pooled it, 156 citations in OpenAlex.
- Epigenetic Mechanisms in Type 2 Diabetes Retinopathy: A Systematic Review.International journal of molecular sciences · 2021Pooled it
- Dysfunction of the Neurovascular Unit in Diabetic Retinopathy: Advances from Molecular Mechanisms to Targeted Interventions.Stem cell reviews and reports · 2026Review
- Retina-specific long non-coding RNAs associated with inherited retinal disease genes.Cellular and molecular life sciences : CMLS · 2026Article
- Epigenetic regulation in type II diabetes: linking molecular mechanisms to clinical management.Journal of diabetes and metabolic disorders · 2026Review
- LncRNA MALAT1 drives diabetic kidney injury via Nrf2 suppression in glomerular endothelium.Scientific reports · 2026Article
- In silico analysis of MALAT1 and H19 lncRNA interactions with the diabetes-related proteins ASK1 and YAP1.In silico pharmacology · 2026Article
- Differential epigenetic regulation of glucose-induced alteration of miR-9 in retinal and cardiac endothelial cells.PloS one · 2026Article
- Emerging liposomal therapies for diabetic retinopathy: a review of novel targeting approaches and advances in retinal health outcomes.Drug delivery · 2025Review
- LncRNA MALAT1 knockdown inhibits apoptosis of mouse hippocampus neuron cells with high glucose by Silencing autophagy.BMC endocrine disorders · 2025Article
- Mitochondrial Fragmentation and Long Noncoding RNAInternational journal of molecular sciences · 2025Article
- Review
- Research Hotspots and Trends of RNA Research in Diabetic Retinopathy: Insights From Bibliometric Analysis.Endocrine, metabolic & immune disorders drug targets · 2025Review
- Inflammation-Induced Klotho Deficiency: A Possible Key Driver of Chronic Kidney Disease Progression.International journal of general medicine · 2025Review
- Use of serum long non-coding RNA expression panel as a marker for diabetic retinopathy.Frontiers in cardiovascular medicine · 2025Article
- Diabetic neuropathy: A NRF2 disease?Journal of diabetes · 2024Review
- Role of long noncoding RNAs in diabetes-associated peripheral arterial disease.Cardiovascular diabetology · 2024Review
- Long Noncoding RNA MALAT1: Salt-Sensitive Hypertension.International journal of molecular sciences · 2024Review
- Relationship between Biochemical Pathways and Non-Coding RNAs Involved in the Progression of Diabetic Retinopathy.Journal of clinical medicine · 2024Review
- Potential roles of lncRNA MALAT1-miRNA interactions in ocular diseases.Journal of cell communication and signaling · 2023Review
- Non-coding RNA-mediated endothelial-to-mesenchymal transition in human diabetic cardiomyopathy, potential regulation by DNA methylation.Cardiovascular diabetology · 2023Article
25 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Despite possessing limited protein-coding potential, long non-coding RNAs (lncRNAs) have been implicated in a myriad of pathologic conditions. Most well documented in cancer, one prominent intergenic lncRNA known as MALAT1 is notorious for its role in impacting epigenetic mechanisms. In this study, we established a novel epigenetic paradigm for MALAT in diabetic retinopathy (DR) by employing siRNA-mediated MALAT1 knockdown in human retinal endothelial cells (HRECs), a Malat1 knockout animal model, vitreous humor from diabetic patients, pharmacological inhibitors for histone and DNA methylation, RNA immunoprecipitation, western blotting, and a unique DNA methylation array to determine glucose-related alterations in MALAT1. Our findings indicated that MALAT1 is capable of impacting the expressions of inflammatory transcripts through its association with components of the PRC2 complex in diabetes. Furthermore, the vitreous humors from diabetic patients revealed increased expressions of MALAT1, TNF-α, and IL-6. Intriguingly, our DNA methylation array demonstrated that transient high glucose exposure in HRECs does not contribute to significant methylation alterations at CpG sites across the MALAT1 gene. However, global inhibition of DNA methyltransferases induced significant increases in MALAT1 and associated inflammatory transcripts in HRECs. Our findings collectively demonstrate the importance of MALAT1 in inflammation and epigenetic regulation in DR.
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