ArticleEBioMedicine2019
MicroRNA let-7-TGFBR3 signalling regulates cardiomyocyte apoptosis after infarction.
Article in EBioMedicine, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed, 46 citations in OpenAlex.
- Apoptotic bodies derived from human umbilical cord mesenchymal stem cells improve recovery from myocardial infarction in swine.Autophagy · 2026Article
- Exploring TGFBR3 in disease pathogenesis: Mechanisms, clinical implications, and pharmacological modulation.Journal of pharmaceutical analysis · 2026Review
- Unraveling Let-7f in oncology: a tumor suppressor with emerging clinical significance.Frontiers in cell and developmental biology · 2026Review
- Knockdown of TGFB2 Attenuates Ischemic Heart Failure by Inhibiting Apoptosis.Cardiovascular toxicology · 2025Article
- Analysis of Differentially Expressed Murine miRNAs in Acute Myocardial Infarction and Target Genes Related to Heart Rate.Cell biochemistry and biophysics · 2025Article
- Activins and Inhibins in Cardiovascular Pathophysiology.Biomolecules · 2024Review
- Mining of potentially stem cell-related miRNAs in planarians.Molecular biology reports · 2024Review
- ExosomalJournal of Zhejiang University. Science. B · 2024Article
- Fibroblast-derived extracellular vesicles as trackable efficient transporters of an experimental nanodrug with fibrotic heart and lung targeting.Theranostics · 2024Article
- Biochemical Structure and Function of TRAPP Complexes in the Cardiac System.JACC. Basic to translational science · 2023Article
- Exosome-derived circ_0001785 delays atherogenesis through the ceRNA network mechanism of miR-513a-5p/TGFBR3.Journal of nanobiotechnology · 2023Article
- Epigenetic modifier alpha-ketoglutarate modulates aberrant gene body methylation and hydroxymethylation marks in diabetic heart.Epigenetics & chromatin · 2023Article
- Review
- Cell-Based and Selected Cell-Free Therapies for Myocardial Infarction: How Do They Compare to the Current Treatment Options?International journal of molecular sciences · 2022Review
- Diagnostic Performance of Circulating miRNAs and Extracellular Vesicles in Acute Ischemic Stroke.International journal of molecular sciences · 2022Article
- Identification of hub genes for adult patients with sepsis via RNA sequencing.Scientific reports · 2022Article
- Systematic Bioinformatics Analysis Based on Public and Second-Generation Sequencing Transcriptome Data: A Study on the Diagnostic Value and Potential Mechanisms of Immune-Related Genes in Acute Myocardial Infarction.Frontiers in cardiovascular medicine · 2022Article
- Protocatechuic aldehyde protects cardiomycoytes against ischemic injuryActa pharmaceutica Sinica. B · 2021Article
- MicroRNAs-The Heart of Post-Myocardial Infarction Remodeling.Diagnostics (Basel, Switzerland) · 2021Review
- MiR-467a-5p aggravates myocardial infarction by modulating ZEB1 expression in mice.Journal of molecular histology · 2021Article
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Authors and funding
16 authors at 7 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundMyocardial infarction (MI) is a life-threatening disease, often leading to heart failure. Defining therapeutic targets at an early time point is important to prevent heart failure.
methodsMicroRNA screening was performed at early time points after MI using paired samples isolated from the infarcted and remote myocardium of pigs. We also examined the microRNA expression in plasma of MI patients and pigs. For mechanistic studies, AAV9-mediated microRNA knockdown and overexpression were administrated in mice undergoing MI.
findingsMicroRNAs let-7a and let-7f were significantly downregulated in the infarct area within 24 h post-MI in pigs. We also observed a reduction of let-7a and let-7f in plasma of MI patients and pigs. Inhibition of let-7 exacerbated cardiomyocyte apoptosis, induced a cardiac hypertrophic phenotype, and resulted in worsened left ventricular ejection fraction. In contrast, ectopic let-7 overexpression significantly reduced those phenotypes and improved heart function. We then identified TGFBR3 as a target of let-7, and found that induction of Tgfbr3 in cardiomyocytes caused apoptosis, likely through p38 MAPK activation. Finally, we showed that the plasma TGFBR3 level was elevated after MI in plasma of MI patients and pigs.
interpretationTogether, we conclude that the let-7-Tgfbr3-p38 MAPK signalling plays an important role in cardiomyocyte apoptosis after MI. Furthermore, microRNA let-7 and Tgfbr3 may serve as therapeutic targets and biomarkers for myocardial damage. FUND: Ministry of Science and Technology, National Health Research Institutes, Academia Sinica Program for Translational Innovation of Biopharmaceutical Development-Technology Supporting Platform Axis, Thematic Research Program and the Summit Research Program, Taiwan.
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