ArticleScientific reports2021
The miRNA199a/SIRT1/P300/Yy1/sST2 signaling axis regulates adverse cardiac remodeling following MI.
Article in Scientific reports, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 36 citations in OpenAlex.
- Early detection value of miR-29a in patients with acute myocardial infarction.Frontiers in cardiovascular medicine · 2026Trial
- Temporal dynamics of cardiac biomarkers in therapy‑related cardiotoxicity: a prospective cardio‑oncology cohort study.Cardio-oncology (London, England) · 2026Article
- Improvement of Number 2 Feibi Recipe on pulmonary fibrosis in mice by inhibiting the level of miR-199a-5p and activating autophagy.Scientific reports · 2025Article
- The Adipokine Hypothesis of Heart Failure With a Preserved Ejection Fraction: A Novel Framework to Explain Pathogenesis and Guide Treatment.Journal of the American College of Cardiology · 2025Review
- miR-106b-5p as a Central Regulator of Cancer Progression and Chemotherapy-Induced Cardiotoxicity: From Molecular Mechanisms to Clinical Translation.International journal of molecular sciences · 2025Review
- miR-199a-5p inhibited HIF-1α to suppress the proliferation, migration, and differentiation of cardiac stem cells.European journal of histochemistry : EJH · 2025Article
- The diagnostic and prognostic value of serum miR-199a-5p combined with echocardiography in acute myocardial infarction.Journal of cardiothoracic surgery · 2025Article
- The Role of Sirtuins in Diabetic Nephropathy: A Comprehensive Review.Current protein & peptide science · 2025Review
- Proregenerative MicroRNAs to Repair the Damaged Heart.European cardiology · 2025Review
- SIRT1: The first key to unlocking the mystery of cardiovascular diseases.Frontiers in pharmacology · 2025Review
- Sex Differences in Expression of Pro-Inflammatory Markers and miRNAs in a Mouse Model of CVB3 Myocarditis.International journal of molecular sciences · 2024Article
- RUNX3-activated apelin signaling inhibits cell proliferation and fibrosis in diabetic nephropathy by regulation of the SIRT1/FOXO pathway.Diabetology & metabolic syndrome · 2024Article
- Advances in research on molecular markers in immune checkpoint inhibitor-associated myocarditis.Cancer innovation · 2023Review
- The Effects of MicroRNAs in the Development of Heart Failure.Current cardiology reports · 2023Review
- Interaction between SIRT1 and non-coding RNAs in different disorders.Frontiers in genetics · 2023Review
- Regulation of HIF-1 by MicroRNAs in Various Cardiovascular Diseases.Current cardiology reviews · 2023Article
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Authors and funding
6 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Left ventricular remodeling following myocardial infarction (MI) is related to adverse outcome. It has been shown that an up-regulation of plasma soluble ST2 (sST2) levels are associated with lower pre-discharge left ventricular (LV) ejection fraction, adverse cardiovascular outcomes and mortality outcome after MI. The mechanisms involved in its modulation are unknown and there is not specific treatment capable of lowering plasma sST2 levels in acute-stage HF. We recently identified Yin-yang 1 (Yy1) as a transcription factor related to circulating soluble ST2 isoform (sST2) expression in infarcted myocardium. However, the underlying mechanisms involved in this process have not been thoroughly elucidated. This study aimed to evaluate the pathophysiological implication of miR-199a-5p in cardiac remodeling and the expression of the soluble ST2 isoform. Myocardial infarction (MI) was induced by permanent ligation of the left anterior coronary artery in C57BL6/J mice that randomly received antimiR199a therapy, antimiR-Ctrl or saline. A model of biomechanical stretching was also used to characterize the underlying mechanisms involved in the activation of Yy1/sST2 axis. Our results show that the significant upregulation of miR-199a-5p after myocardial infarction increases pathological cardiac hypertrophy by upregulating circulating soluble sST2 levels. AntimiR199a therapy up-regulates Sirt1 and inactivates the co-activator P300 protein, thus leading to Yy1 inhibition which decreases both expression and release of circulating sST2 by cardiomyocytes after myocardial infarction. Pharmacological inhibition of miR-199a rescues cardiac hypertrophy and heart failure in mice, offering a potential therapeutic approach for cardiac failure.
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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 Socratic graph.