ArticleMediators of inflammation2015
MicroRNA-208a Dysregulates Apoptosis Genes Expression and Promotes Cardiomyocyte Apoptosis during Ischemia and Its Silencing Improves Cardiac Function after Myocardial Infarction.
Article in Mediators of inflammation, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 52 citations in OpenAlex.
- Advances in MicroRNA-Based Therapies for Cardiac Repair: Emerging Strategies for Treating Myocardial Infarction.Molecular and cellular biochemistry · 2026Review
- MiR-206 may regulate mitochondrial ROS contribute to the progression of Myocardial infarction via TREM1.BMC cardiovascular disorders · 2023Article
- All roads lead to Rome - a review of the potential mechanisms by which exerkines exhibit neuroprotective effects in Alzheimer's disease.Neural regeneration research · 2022Review
- Molecular mechanisms of isoflavone puerarin against cardiovascular diseases: What we know and where we go.Chinese herbal medicines · 2022Review
- MiR-208b/miR-21 Promotes the Progression of Cardiac Fibrosis Through the Activation of the TGF-β1/Smad-3 Signaling Pathway: AnFrontiers in cardiovascular medicine · 2022Article
- Construction of miRNA-mRNA network reveals crucial miRNAs and genes in acute myocardial infarction.Journal of biomedical research · 2021Article
- Current Knowledge of MicroRNAs (miRNAs) in Acute Coronary Syndrome (ACS): ST-Elevation Myocardial Infarction (STEMI).Life (Basel, Switzerland) · 2021Review
- AKR1C3 and Its Transcription Factor HOXB4 Are Promising Diagnostic Biomarkers for Acute Myocardial Infarction.Frontiers in cardiovascular medicine · 2021Article
- Deficiency of miR-208a Exacerbates CClHepatology communications · 2020Article
- Modulation of MicroRNAs as a Potential Molecular Mechanism Involved in the Beneficial Actions of Physical Exercise in Alzheimer Disease.International journal of molecular sciences · 2020Review
- Role of MicroRNAs in Diagnosis, Prognosis, and Treatment of Acute Heart Failure: Ambassadors from Intracellular Zone.Galen medical journal · 2020Review
- Role of miRNAs on the Pathophysiology of Cardiovascular Diseases.Arquivos brasileiros de cardiologia · 2018Review
- Non-coding RNAs as biomarkers for acute myocardial infarction.Acta pharmacologica Sinica · 2018Review
- MiR-33 promotes myocardial fibrosis by inhibiting MMP16 and stimulating p38 MAPK signaling.Oncotarget · 2018Article
- miR-190 protects cardiomyocytes from apoptosis induced by HInternational journal of clinical and experimental pathology · 2018Article
- Abnormal expression of long non-coding RNAs in myocardial infarction.Heart and vessels · 2017Article
- Cardioprotective effect of Notch signaling on the development of myocardial infarction complicated by diabetes mellitus.Experimental and therapeutic medicine · 2017Article
- Extracellular vesicles-mediated transfer of miR-208a/b exaggerate hypoxia/reoxygenation injury in cardiomyocytes by reducing QKI expression.Molecular and cellular biochemistry · 2017Article
- Differential expression of microRNAs following cardiopulmonary bypass in children with congenital heart diseases.Journal of translational medicine · 2017Article
- Regulatory non-coding RNAs in acute myocardial infarction.Journal of cellular and molecular medicine · 2017Review
Corrections and comments
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Authors and funding
7 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
aimsmiR-208a is associated with adverse outcomes in several cardiac pathologies known to have increased apoptosis, including myocardial infarction (MI). We investigated if miR-208a has proapoptotic effects on ischemic cardiomyocytes and if its silencing has therapeutic benefits in MI. METHODS AND
resultsThe effect of miR-208a on apoptosis during ischemia was studied in cultured neonatal mice myocytes transfected with agomir or antagomir. Differential gene expression was assessed using microarrays. MI was induced in male C57BL/6 mice randomly assigned to antagomir (n = 6) or control group (n = 7), while sham group (n = 7) had sham operation done. Antagomir group received miR208a antagomir, while control and sham group mice received vehicle only. At 7 and 28 days, echocardiography was done and thereafter hearts were harvested for analysis of apoptosis by TUNEL method, fibrosis using Masson's trichrome, and hypertrophy using hematoxylin and eosin. miR-208a altered apoptosis genes expression and increased apoptosis in ischemic cardiomyocytes. Therapeutic inhibition of miR-208a decreased cardiac fibrosis, hypertrophy, and apoptosis and significantly improved cardiac function 28 days after MI.
conclusionmiR-208a alters apoptosis genes expression and promotes apoptosis in ischemic cardiomyocytes, and its silencing attenuates apoptosis, fibrosis, and hypertrophy after MI, with significant improvement in cardiac function.
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