ArticleCell death & disease2017
lncRNA MIAT functions as a competing endogenous RNA to upregulate DAPK2 by sponging miR-22-3p in diabetic cardiomyopathy.
Article in Cell death & disease, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 122 papers, 3 of them syntheses that pooled it.
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Who cites it
122 citing papers in PubMed, 3 syntheses or guidelines pooled it, 203 citations in OpenAlex.
- From Type 2 Diabetes Mellitus To Diabetic Cardiomyopathy - A Systematic Review On The Role Of MicroRNA.Current diabetes reports · 2025Pooled it
- The role of DAPK2 as a key regulatory element in various human cancers: a systematic review.Molecular biology reports · 2024Pooled it
- The Impact of lncRNAs in Diabetes Mellitus: A Systematic Review andFrontiers in endocrinology · 2021Pooled it
- BACH2 links β1-adrenergic receptor/β-arrestin1 signaling to MIAT to inhibit cardiac fibroblast activation and cardiomyocyte apoptosis.Cell death discovery · 2026Article
- MIAT: An important long non-coding RNA regulating cardiovascular and cerebrovascular diseases.Frontiers in cardiovascular medicine · 2026Review
- Circular RNAs as Biomarkers and Therapeutic Targets in Diabetic Cardiovascular Complications.Endocrinology, diabetes & metabolism · 2026Review
- The impact of ncRNAs on type 2 diabetes: A comprehensive review covering molecular mechanisms to clinical applications.Molecular therapy. Nucleic acids · 2025Review
- Established and Emerging Roles of Epigenetic Regulation in Diabetic Cardiomyopathy.Diabetes/metabolism research and reviews · 2025Review
- A comprehensive review on diabetic cardiomyopathy (DCM): histological spectrum, diagnosis, pathogenesis, and management with conventional treatments and natural compounds.Naunyn-Schmiedeberg's archives of pharmacology · 2025Review
- Hepatitis B virus core/capsid protein induces hepatocellular carcinoma progression via long non-coding RNA KCNQ1OT1/miR-335-5p/CDC7 axis.Translational cancer research · 2025Article
- Long noncoding RNAs in familial hypercholesterolemia: biomarkers, therapeutics, and AI in precision medicine.Lipids in health and disease · 2025Review
- MIAT: A pivotal oncogenic long noncoding RNA tunning the hallmarks of solid malignancies.Translational oncology · 2025Article
- Cardiomyocyte-restricted MIAT deletion is sufficient to protect against murine myocardial infarction.Cell death discovery · 2025Article
- Investigate of LOC101928988 Regulatory Effect on the DAPK2 Transcription in Breast Tumors.Cancer reports (Hoboken, N.J.) · 2025Article
- Identification of hub genes in myocardial infarction by bioinformatics and machine learning: insights into inflammation and immune regulation.Frontiers in molecular biosciences · 2025Article
- The interregulatory circuit between non-coding RNA and apoptotic signaling in diabetic cardiomyopathy.Non-coding RNA research · 2024Review
- Importance of long non-coding RNAs in the pathogenesis, diagnosis, and treatment of myocardial infarction.International journal of cardiology. Heart & vasculature · 2024Review
- The study of the mechanism of non-coding RNA regulation of programmed cell death in diabetic cardiomyopathy.Molecular and cellular biochemistry · 2024Review
- Roles of non-coding RNA in diabetic cardiomyopathy.Cardiovascular diabetology · 2024Review
- Review
62 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
We previously established a rat model of diabetic cardiomyopathy (DCM) and found that the expression of long non-coding RNA myocardial infarction-associated transcript (MIAT) was significantly upregulated. The present study was aimed to determine the pathologic role of MIAT in the development of DCM. MIAT knockdown was found to reduce cardiomyocyte apoptosis and improve left ventricular function in diabetic rats. High glucose could increase MIAT expression and induce apoptosis in cultured neonatal cardiomyocytes. The results of luciferase reporter assay and RNA immunoprecipitation assay revealed that MIAT was targeted by miR-22-3p in an AGO2-dependent manner. In addition, the 3'-untranslated region of DAPK2 was fused to the luciferase coding region and transfected into HEK293 cells with miR-22-3p mimic, and the results showed that DAPK2 was a direct target of miR-22-3p. Our findings also indicated that MIAT overexpression could counteract the inhibitory effect of miR-22-3p on DAPK2. Moreover, MIAT knockdown was found to reduce DAPK2 expression and inhibit apoptosis in cardiomyocytes exposed to high glucose. In conclusion, our study demonstrates that MIAT may function as a competing endogenous RNA to upregulate DAPK2 expression by sponging miR-22-3p, which consequently leads to cardiomyocyte apoptosis involved in the pathogenesis of DCM.
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