ArticleBiotechnology letters2021
miR-19a mitigates hypoxia/reoxygenation-induced injury by depressing CCL20 and inactivating MAPK pathway in human embryonic cardiomyocytes.
Article in Biotechnology letters, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers, 1 of them a synthesis that pooled it.
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Who cites it
5 citing papers in PubMed, 1 synthesis or guideline pooled it, 6 citations in OpenAlex.
- Potential role of a three-gene signature in predicting diagnosis in patients with myocardial infarction.Bioengineered · 2021Pooled it
- GABARAPL1 Exerts Regulatory Effects on Hypoxia-Induced Pyroptosis in the Pathogenesis of Myocardial Infarction.Journal of cellular and molecular medicine · 2025Article
- Expression levels and clinical significance of serum miR-19a/CCL20 in patients with acute cerebral infarction.Open medicine (Warsaw, Poland) · 2024Article
- Ssc-miR-141 Attenuates Hypoxia-Induced Alveolar Type II Epithelial Cell Injury in Tibetan Pigs by TargetingGenes · 2022Article
- Effects of chronic hypoxia on the gene expression profile in the embryonic heart in three Chinese indigenous chicken breeds (Frontiers in veterinary science · 2022Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectiveMyocardial infarction (MI) is a prevalent cardiovascular puzzle and a mainspring of disease-induced mortality. We performed this investigation to detect the role of putative important miRNAs or genes in MI.
resultsCCL20 may be a potential therapeutic target, which was directly targeted and negatively regulated by miR-19a. CCL20 expression was significantly increased in MI tissue samples, but miR-19a was expressed at lower levels in MI. H/R treatment inhibited cell viability and induced an increase of apoptotic rate compared with Sham group. However, miR-19a mimic relieved the H/R-stimulated injury to cardiomyocytes. Protective effect of miR-19a against H/R in cardiomyocytes was reversed by CCL20 enhancement, and MAPK pathway was inactivated during this progression.
conclusionsmiR-19a eliminates the H/R-induced injury in cardiomyocytes through directly targeting CCL20 and attenuating the activity of MAPK signaling pathway. These observations highlighted the therapeutic roles of miR-19a and CCL20 for MI treatment.
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