ArticleCirculation. Heart failure2022
MiR-150 Attenuates Maladaptive Cardiac Remodeling Mediated by Long Noncoding RNA MIAT and Directly Represses Profibrotic
Article in Circulation. Heart failure, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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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.
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Who cites it
28 citing papers in PubMed, 32 citations in OpenAlex.
- Review
- Identification of miR-150-5p in Human Amniotic Membrane Mesenchymal Cell-Derived Extracellular Vesicles as a Novel Mechanism Driving Cardioprotection.European journal of clinical investigation · 2026Article
- BACH2 links β1-adrenergic receptor/β-arrestin1 signaling to MIAT to inhibit cardiac fibroblast activation and cardiomyocyte apoptosis.Cell death discovery · 2026Article
- The European BestAgeing Study on microRNA candidates reveals distinct signatures with diagnostic and prognostic potential in cardiovascular disease.BMC medicine · 2025Article
- Overview of exosomal non-coding RNAs in cardiovascular disease using high throughput sequencing.European journal of pharmacology · 2025Review
- Role of Homeobox (HOX) Genes in Adult Cardiovascular Disease: From Developmental Regulators to Therapeutic Targets.Cureus · 2025Review
- Differential Expression of LncRNA MIAT and Its Clinical Significance in Intracranial Aneurysms.Brain and behavior · 2025Article
- The relationship between oral burns and oral squamous cell carcinoma: a systematic review.Annals of medicine and surgery (2012) · 2025Article
- Cardiomyocyte-restricted MIAT deletion is sufficient to protect against murine myocardial infarction.Cell death discovery · 2025Article
- MicroRNA-150 Deletion from Adult Myofibroblasts Augments Maladaptive Cardiac Remodeling Following Chronic Myocardial Infarction.Biomolecules · 2024Article
- Epigenetic Study of Cohort of Monozygotic Twins With Hypertrophic Cardiomyopathy Due to MYBPC3 (Cardiac Myosin-Binding Protein C).Journal of the American Heart Association · 2024Article
- Non-Coding RNA-Mediated Gene Regulation in Cardiovascular Disorders: Current Insights and Future Directions.Journal of cardiovascular translational research · 2024Review
- Non-coding RNAs as therapeutic targets and biomarkers in ischaemic heart disease.Nature reviews. Cardiology · 2024Review
- Long non-coding RNAs in cardiac hypertrophy and heart failure: functions, mechanisms and clinical prospects.Nature reviews. Cardiology · 2024Review
- Role of HOXA1-4 in the development of genetic and malignant diseases.Biomarker research · 2024Review
- Deciphering the emerging landscape of HOX genes in cardiovascular biology, atherosclerosis and beyond (Review).International journal of molecular medicine · 2024Article
- LIPCAR levels in plasma-derived extracellular vesicles is associated with left ventricle remodeling post-myocardial infarction.Journal of translational medicine · 2024Article
- Clinical Variables Influence the Ability of miR-101, miR-150, and miR-21 to Predict Ventricular Remodeling after ST-Elevation Myocardial Infarction.Biomedicines · 2023Article
- Epigenome-wide association study using peripheral blood leukocytes identifies genomic regions associated with periodontal disease and edentulism in the Atherosclerosis Risk in Communities study.Journal of clinical periodontology · 2023Article
- Plasma lncRNA LIPCAR Expression Levels Associated with Neurological Impairment and Stroke Subtypes in Patients with Acute Cerebral Infarction: A Prospective Observational Study with a Control Group.Neurology and therapy · 2023Article
Corrections and comments
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Authors and funding
13 authors at 5 institutions in 2 countries.
Funding
Abstract
backgroundMicroRNA-150 (miR-150) plays a protective role in heart failure (HF). Long noncoding RNA, myocardial infarction-associated transcript (MIAT) regulates miR-150 function in vitro by direct interaction. Concurrent with miR-150 downregulation, MIAT is upregulated in failing hearts, and gain-of-function single-nucleotide polymorphisms in MIAT are associated with increased risk of myocardial infarction (MI) in humans. Despite the correlative relationship between MIAT and miR-150 in HF, their in vivo functional relationship has never been established, and molecular mechanisms by which these 2 noncoding RNAs regulate cardiac protection remain elusive.
methodsWe use MIAT KO (knockout),
resultsUsing novel mouse models, we demonstrate that genetic overexpression of MIAT worsens cardiac remodeling, while genetic deletion of MIAT protects hearts against MI. Importantly, miR-150 overexpression attenuates the detrimental post-MI effects caused by MIAT. Genome-wide transcriptomic analysis of MIAT null mouse hearts identifies
conclusionsOur findings delineate a pivotal functional interaction among MIAT, miR-150, and
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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.