ArticleMammalian genome : official journal of the International Mammalian Genome Society2021
TUG1 knockdown suppresses cardiac fibrosis after myocardial infarction.
Article in Mammalian genome : official journal of the International Mammalian Genome Society, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 17 citations in OpenAlex.
- Long Non-coding RNA Taurine Up-regulated Gene 1 Exacerbates Cardiac Fibrosis and Cardiomyocyte Apoptosis After Acute Myocardial Infarction by Modulating the MicroRNA-27a-3p/Zinc-finger Protein 36 Axis.Applied biochemistry and biotechnology · 2026Article
- LncRNA TUG1 promotes hypertrophic scar formation via the miR-627/IGF1R axis.Journal of molecular histology · 2026Article
- Importance of long non-coding RNAs in the pathogenesis, diagnosis, and treatment of myocardial infarction.International journal of cardiology. Heart & vasculature · 2024Review
- Characterization of global research trends and prospects on sudden coronary death: A literature visualization analysis.Heliyon · 2023Article
- The Role of ncRNAs in Cardiac Infarction and Regeneration.Journal of cardiovascular development and disease · 2023Review
- lncRNA TUG1 regulates hyperuricemia-induced renal fibrosis in a rat model.Acta biochimica et biophysica Sinica · 2022Article
- Analysis of susceptibility genes and myocardial infarction risk correlation of ischemic cardiomyopathy based on bioinformatics.Journal of thoracic disease · 2022Article
- New developments in the biology of fibroblast growth factors.WIREs mechanisms of disease · 2022Review
- Post-Transcriptional Regulation of Molecular Determinants during Cardiogenesis.International journal of molecular sciences · 2022Review
- Construction of the ceRNA network in the progression of acute myocardial infarction.American journal of cardiovascular disease · 2022Article
- The Regulation Mechanisms and Clinical Application of MicroRNAs in Myocardial Infarction: A Review of the Recent 5 Years.Frontiers in cardiovascular medicine · 2021Review
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cardiac fibrosis is involved in myocardial remodeling following acute myocardial infarction (AMI), which can result in heart failure, arrhythmias and even sudden cardiac death. Investigating the molecular mechanisms of cardiac fibrosis in acute myocardial infarction (AMI) is essential for better understanding this pathology. The current study aims to investigate the effect of TUG1 on cardiac fibrosis after AMI and elucidated the underlying molecular mechanism of AMI. Rats were randomly divided into four groups (sham-operation group, myocardial infarction group (AMI group), si-NC treated group and si-TUG1 treated group). The biological behavior of cardiac fibroblasts treated with TGF-β1after being transfected by si-TUG1 or miR-590 mimic or miR-590 inhibitor or FGF1 mimic or a combination was evaluated using the cell counting kit-8 (CCK8) and Transwell assays. SatarBase v2.0 was used to predict the target microRNAs binding site candidates with TUG1 and FGF1. Western blot and recovery experiments were used to explore the potential mechanism. TUG1 expression was up-regulated and knockdown of TUG1 improved cardiac function in AMI rats. Knockdown of TUG1 suppressed cell viability and migration and improved collagen production of TGF-β1 treated cardiac fibroblasts. SatarBase v2.0 showed TUG1 served as a sponge for miR-590 and FGF1 is a direct target of miR-590. TUG1 expression was increased in AMI tissue and cardiac fibroblasts treated with TGF-β1. TUG1 knockdown suppressed the biological process of cardiac fibroblasts treated with TGF-β1 by sponging miR-590.
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