ArticlePeerJ2023
RUNX1 facilitates heart failure progression through regulating TGF-β-induced cardiac remodeling.
Article in PeerJ, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 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.
The trial behind it
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Who cites it
8 citing papers in PubMed, 14 citations in OpenAlex.
- SOX2-OT serves as a diagnostic and prognostic biomarker for hypertensive left ventricular hypertrophy by targeting miR-30d-5p.Molecular and cellular biochemistry · 2026Article
- Targeting RUNX1 protects against diastolic dysfunction in a two-hit mouse model of heart failure with preserved ejection fraction.Cardiovascular research · 2026Article
- Identification of RUNX1 as a Biomarker for Right Ventricular Remodeling in Pulmonary Arterial Hypertension Using WGCNA.Pulmonary circulation · 2026Article
- Circulating microRNAs miR-21-5p, miR-23a-3p and miR-26a-5p reflect clinical and molecular features of aging.Scientific reports · 2025Article
- A novel cardiomyopathy phenotype linked to a CHD7 missense variant.Scientific reports · 2025Article
- Review
- A novel bioactive peptide-peptoid hybrid of alpha-calcitonin gene-related peptide protects against pressure-overload induced heart failure.Frontiers in pharmacology · 2025Article
- The role of IFI16 in regulating PANoptosis and implication in heart diseases.Cell death discovery · 2024Review
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
Background: Heart failure is caused by acute or chronic cardiovascular diseases with limited treatments and unclear pathogenesis. Therefore, it is urgent to explore new therapeutic targets and reveal new pathogenesis for heart failure. Methods: We carried out heart failure animal model by transverse aortic arch constriction (TAC) in mice. The left ventricular internal diameter diastole (LVIDd), left ventricular internal diameter systole (LVIDs), and ejection fraction (EF) value were detected using ultrasound and myocardial fibrosis was evaluated by Masson stain assay. Cell apoptosis in myocardial tissues were detected by TUNEL immunofluorescence stain. Signal pathway analysis was performed by dual-luciferase reporter assay and western blot. Results: Our results showed that inhibition of RUNX1 led to remission of cardiac enlargement induced by TAC in mice. Inhibition of RUNX1 also caused raise of EF and FS value under TAC-induced condition. Besides, RUNX1 inhibition mice showed decreased myocardial fibrosis area under TAC-induced condition. RUNX1 inhibition caused decrease of apoptotic cell rate in myocardial tissues under TAC. Interestingly, we found that RUNX1 could promote the activation of TGF-β/Smads in dual-luciferase reporter assay. Interpretation: We illustrated that RUNX1 could be considered as a new regulator of myocardial remodeling by activating TGF-β/Smads signaling. Based on this, we concluded that RUNX1 may be developed as a new therapeutic target against heart failure in the future. In addition, this study also provide a new insight for the etiological study on heart failure.
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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 Socratic graph.