ArticleMolecular therapy. Nucleic acids2019
Simultaneous Suppression of Multiple Programmed Cell Death Pathways by miRNA-105 in Cardiac Ischemic Injury.
Article in Molecular therapy. Nucleic acids, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 32 citations in OpenAlex.
- Article
- epHero - a tandem-fluorescent probe to track the fate of apoptotic cells during efferocytosis.Cell death discovery · 2024Article
- Exploring Cardiac Exosomal RNAs of Acute Myocardial Infarction.Biomedicines · 2024Article
- MicroRNA profiling of the feline left heart identifies chamber-specific expression signatures in health and in advanced hypertrophic cardiomyopathy.Journal of molecular and cellular cardiology plus · 2023Article
- Vagus nerve stimulation exerts cardioprotection against doxorubicin-induced cardiotoxicity through inhibition of programmed cell death pathways.Cellular and molecular life sciences : CMLS · 2022Article
- The regulation of necroptosis and perspectives for the development of new drugs preventing ischemic/reperfusion of cardiac injury.Apoptosis : an international journal on programmed cell death · 2022Review
- MicroRNA-26a/b-5p promotes myocardial infarction-induced cell death by downregulating cytochrome c oxidase 5a.Experimental & molecular medicine · 2021Article
- Advances in the mechanism and treatment of mitochondrial quality control involved in myocardial infarction.Journal of cellular and molecular medicine · 2021Review
- Cell type-specific microRNA therapies for myocardial infarction.Science translational medicine · 2021Review
- Astragaloside IV Ameliorates Myocardial Infarction Induced Apoptosis and Restores Cardiac Function.Frontiers in cell and developmental biology · 2021Article
- Neutrophil-Mediated Cardiac Damage After Acute Myocardial Infarction: Significance of Defining a New Target Cell Type for Developing Cardioprotective Drugs.Antioxidants & redox signaling · 2020Article
- Circulating microRNA profiles based on direct S-Poly(T)Plus assay for detection of coronary heart disease.Journal of cellular and molecular medicine · 2020Article
- Intracerebral hemorrhage alters circular RNA expression profiles in the rat brain.American journal of translational research · 2020Article
- MiR-149 Aggravates Pyroptosis in Myocardial Ischemia-Reperfusion Damage via Silencing FoxO3.Medical science monitor : international medical journal of experimental and clinical research · 2019Article
- miR-499 released during myocardial infarction causes endothelial injury by targeting α7-nAchR.Journal of cellular and molecular medicine · 2019Article
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Authors and funding
12 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Recent studies have shown that several upstream signaling elements of apoptosis and necroptosis are closely associated with acute injury in the heart. In our study, we observed that miR-105 was notably dysregulated in rat hearts with myocardial infarction (MI). Thus, the purpose of this study was to test the hypothesis that miR-105 participates in the regulation of RIP3/p-MLKL- and BNIP3-dependent necroptosis/apoptosis in H9c2 cells and MI rat hearts. Our results show that the RIP3/p-MLKL necroptotic pathway and BNIP3-dependent apoptosis signaling are enhanced in H9c2 cells under hypoxic conditions, whereas, compared with these pathways in the controls, those in miR-105-treated H9c2 cells are suppressed. Mechanistically, we identified miR-105 as the miRNA directly suppressing the expression of RIP3 and BNIP3, two important mediators involved in cell necroptosis and apoptosis. Furthermore, MI rat hearts injected with miR-105 had decreased infarct sizes, indicating that miR-105 is among three miRNAs that function simultaneously to suppress necroptotic/apoptotic cell death pathways and to inhibit MI-induced cardiomyocyte cell death at multiple levels. Taken together, miR-105 may constitute a new therapeutic strategy for cardioprotection in ischemic heart disease.
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