ArticleThe Journal of international medical research2021
The mechanism of myocardial fibrosis is ameliorated by myocardial infarction-associated transcript through the PI3K/Akt signaling pathway to relieve heart failure.
Article in The Journal of international medical research, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 26 citations in OpenAlex.
- Machine learning combined with multi-omics analysis: identifying nucleotide metabolism-associated immune genes and validating their functions in cardiomyopathy.BMC cardiovascular disorders · 2026Article
- Article
- Knockdown of FXYD2 inhibits mepivacaine-induced cardiomyocyte injury by activating the PI3K/AKT signaling pathway.European journal of medical research · 2025Article
- Review
- Emerging Roles of Long Non-Coding RNAs in Cardiovascular Diseases.Journal of cellular and molecular medicine · 2025Review
- Review
- Molecular Mechanism of Yangshen Maidong Decoction in the Treatment of Chronic Heart Failure based on Network Pharmacology, Molecular Docking, and Molecular Dynamics Simulations.Cell biochemistry and biophysics · 2024Article
- Activation of AHR by ITE improves cardiac remodelling and function in rats after myocardial infarction.ESC heart failure · 2023Article
- Expression and correlation of the Pi3k/Akt pathway and VEGF in oral submucous fibrosis.Cell proliferation · 2023Article
- Identification of crucial genes related to heart failure based on GEO database.BMC cardiovascular disorders · 2023Article
- Mechanism of angiotensin-converting enzyme inhibitors in the treatment of dilated cardiomyopathy based on a protein interaction network and molecular docking.Cardiovascular diagnosis and therapy · 2023Article
- The Role of ncRNAs in Cardiac Infarction and Regeneration.Journal of cardiovascular development and disease · 2023Review
- Integrated bioinformatics and machine learning algorithms reveal the critical cellular senescence-associated genes and immune infiltration in heart failure due to ischemic cardiomyopathy.Frontiers in immunology · 2023Article
- Anti-apoptotic and anti-fibrotic efficacy of exercise training in hypertensive hearts: A systematic review.Frontiers in cardiovascular medicine · 2023Review
- Non-coding RNAs in the pathophysiology of heart failure with preserved ejection fraction.Frontiers in cardiovascular medicine · 2023Review
- Review
- Natural products of traditional Chinese medicine treat atherosclerosis by regulating inflammatory and oxidative stress pathways.Frontiers in pharmacology · 2022Review
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectiveThis study aimed to investigate the role of long noncoding RNA (LncRNA) myocardial infarction-associated transcript (MIAT) in a heart failure (HF) model
methodsWe established HF models
resultsWe found that when LncRNA MIAT was silenced, vascular endothelial growth factor, phosphorylated protein kinase B (Akt), and phosphorylated phosphoinositide 3-kinase (PI3K) mRNA and protein levels were significantly downregulated, which suggested that MIAT activated the PI3K/Akt signaling pathway. Akt and PI3K expression was not significantly changed. We also found that when LncRNA MIAT was silenced, collagen expression was significantly downregulated. This finding suggested that MIAT promoted myocardial fibrosis during the development of HF. The levels of inflammatory factors were also significantly reduced with silencing of LncRNA MIAT. This finding suggested that MIAT promoted the expression of inflammatory factors in myocardial fibrosis by activating the PI3K/Akt signaling pathway.
conclusionThis study indicates that silencing LncRNA MIAT may improve myocardial fibrosis and alleviate HF through the PI3K/Akt signaling pathway, which may be helpful for patients with HF to obtain a better therapeutic effect.
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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.