ArticleAmerican journal of translational research2020
Inhibition of long non-coding RNA TUG1 protects against diabetic cardiomyopathy induced diastolic dysfunction by regulating miR-499-5p.
Article in American journal of translational research, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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Who cites it
16 citing papers in PubMed, 26 citations in OpenAlex.
- MiR-499-5P/PACS2/TRPV1 Axis Maintains Mitochondrial Homeostasis and Left Ventricular Function after Extreme Cold Stress.Journal of cardiovascular translational research · 2026Article
- Muscle-specific miR-499-5p delivered by small extracellular vesicles impairs endothelial function and ischemic hindlimb recovery in diabetic mice.Cardiovascular diabetology · 2025Article
- Diabetes and diabetic associative diseases: An overview of epigenetic regulations of TUG1.Saudi journal of biological sciences · 2024Review
- LncRNA and mRNA expression characteristic and bioinformatic analysis in myocardium of diabetic cardiomyopathy mice.BMC genomics · 2024Article
- Expression profiles and bioinformatic analysis of microRNAs in myocardium of diabetic cardiomyopathy mice.Genes & genomics · 2023Article
- Cellular interplay between cardiomyocytes and non-myocytes in diabetic cardiomyopathy.Cardiovascular research · 2023Review
- N6-Methyladenosine Methyltransferase METTL3 Alleviates Diabetes-Induced Testicular Damage through Modulating TUG1/Clusterin Axis.Diabetes & metabolism journal · 2023Article
- Effects of non-coding RNAs and RNA-binding proteins on mitochondrial dysfunction in diabetic cardiomyopathy.Frontiers in cardiovascular medicine · 2023Review
- Non-coding RNAs in the pathophysiology of heart failure with preserved ejection fraction.Frontiers in cardiovascular medicine · 2023Review
- Unveiling the Vital Role of Long Non-Coding RNAs in Cardiac Oxidative Stress, Cell Death, and Fibrosis in Diabetic Cardiomyopathy.Antioxidants (Basel, Switzerland) · 2022Review
- Review
- Long noncoding RNA H19 suppresses cardiac hypertrophy through the MicroRNA-145-3p/SMAD4 axis.Bioengineered · 2022Article
- Emerging Role of Long Non-Coding RNAs in Diabetic Vascular Complications.Frontiers in endocrinology · 2021Review
- Long Non-coding RNA: A Key Regulator in the Pathogenesis of Diabetic Cardiomyopathy.Frontiers in cardiovascular medicine · 2021Review
- Knockdown of TUG1 rescues cardiomyocyte hypertrophy through targeting the miR-497/MEF2C axis.Open life sciences · 2021Article
- Emerging crosstalk between long non-coding RNAs and Nrf2 signaling.Cancer letters · 2020Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Reportedly, several long non-coding RNAs (lncRNAs) have been involved in the regulation of cardiac hypertrophy induced by diabetic cardiomyopathy (DCM), causing cardiac dysfunction and subsequent failure. Although lncRNA taurine upregulated gene 1 (TUG1) is associated with myocardial injury, the expression profile and potential role of TUG1 in DCM-related cardiac hypertrophy remain unknown. This study elucidated the functions of TUG1 in DCM and its underlying mechanisms. Our results demonstrated that the expression of TUG1 was upregulated in db/db mice cardiomyocytes. Inhibition of TUG1 by lentivirus si-TUG1 indicated no effect on systolic function; however, it effectively improved DCM-induced diastolic dysfunction in db/db mice. TUG1 silencing demonstrated no influence on the metabolic characteristics of DCM, including blood glucose and lipid levels. Notably, TUG1 knockdown significantly decreased cardiac hypertrophy and reduced the fibrotic area,
Indexed as
Identifiers
32269707PMC7137062W3026743080What OpenQuestion holds
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.