ArticleMolecular biotechnology2022
Hsa-miR-199a-5p Protect Cell Injury in Hypoxia Induces Myocardial Cells Via Targeting HIF1α.
Article in Molecular biotechnology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
6 citing papers in PubMed, 14 citations in OpenAlex.
- miR-199a-5p inhibited HIF-1α to suppress the proliferation, migration, and differentiation of cardiac stem cells.European journal of histochemistry : EJH · 2025Article
- Comprehensive analysis of diagnostic biomarkers related to histone acetylation in acute myocardial infarction.BMC medical genomics · 2025Article
- Analysis of the correlation between the levels of HIF-1α and miR-199a in lesions and the psoriasis severity index.Postepy dermatologii i alergologii · 2024Article
- Article
- MiR-199a-5p enhances neuronal differentiation of neural stem cells and promotes neurogenesis by targeting Cav-1 after cerebral ischemia.CNS neuroscience & therapeutics · 2023Article
- MiR-199a-5p promotes ferroptosis-induced cardiomyocyte death responding to oxygen-glucose deprivation/reperfusion injury via inhibiting Akt/eNOS signaling pathway.The Kaohsiung journal of medical sciences · 2022Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
Myocardial infarction (MI) is one of the most common global diseases. Recently, microRNA 199a-5p (miR-199a-5p) has been recognized as a vital regulator in several human diseases. Nevertheless, the function of miR-199a-5p and the associated downstream molecular mechanisms in myocardial injury remain undescribed. Here, we assessed the relative expression of miR-199a-5p in an oxidative stress injury model of human myocardial cells. The effects of miR-199a-5p on myocardial cell viability were determined by cell counting kit-8 (CCK-8), terminal deoxynucleotidyl transferase UTP nick end labeling (TUNEL), flow cytometry, and western blot assays. Online bioinformatic analysis was used to predict the aim of miR-199a-5p in cardiomyocyte injury, which was confirmed by dual-luciferase reporter assays. miR-199a-5p increased the growth rate of cardiomyocytes after treatment with a hypoxic environment. miR-199a-5p acted as an inhibitor directly targeted hypoxia-inducible factor-1 (HIF1α) expression, which was higher in the cardiomyocyte injury model than that in healthy myocardial cells. Upregulated HIF1α expression abolished miR-199a-5p-induced cell proliferation in the cardiomyocyte hypoxia model. Our results suggest that miR-199a-5p is a potential prognostic biomarker in myocardial damage.
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Registered trials
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