ArticleBMC cardiovascular disorders2020
LncRNAMORT is upregulated in myocardial infarction and promotes the apoptosis of cardiomyocyte by downregulating miR-93.
Article in BMC cardiovascular disorders, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 9 citations in OpenAlex.
- MiRNA-93: a novel signature in human disorders and drug resistance.Cell communication and signaling : CCS · 2023Review
- Long non-coding RNA LUCAT1 inhibits myocardial oxidative stress and apoptosis after myocardial infarction via targeting microRNA-181a-5p.Bioengineered · 2021Article
- LncRNAInternational journal of molecular sciences · 2021Review
- Silencing CircHIPK3 Sponges miR-93-5p to Inhibit the Activation of Rac1/PI3K/AKT Pathway and Improves Myocardial Infarction-Induced Cardiac Dysfunction.Frontiers in cardiovascular medicine · 2021Article
- Targeting Epigenetics and Non-coding RNAs in Myocardial Infarction: From Mechanisms to Therapeutics.Frontiers in genetics · 2021Review
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
backgroundMyocardial infarction (MI) affects the expression of a large number of lncRNAs, while the functions of those dysregulated lncRNAs are mostly unclear. MATERIALS AND
methodsExpression of MORT and miR-93 in hearth tissues and plasma of both MI mice and Sham mice and both MI patients and healthy controls was detected by RT-qPCR. Correlations of expression levels of MORT and miR-93 between hear tissues and plasma of MI mice were explored by performing linear regression.
resultsIn the present study we found that MORT expression levels were higher, while expression levels of miR-93 were lower in both plasma and heart tissues of mice MI mice models compared with Sham mice. Plasma levels of MORT and miR-93 were largely consistent with expression levels of MORT and miR-93 in heart tissue of MI mice. MORT expression levels were also higher, while levels of miR-93 were also lower in plasma of MI patients compared with healthy controls. MORT and miR-93 were inversely correlated in MI patients but not in healthy controls. MORT overexpression resulted in inhibited miR-93 expression in cardiomyocytes (AC16 cell line), while miR-93 overexpression did not significantly affect MORT expression. MORT overexpression promoted cardiomyocyte apoptosis, while miR-93 overexpression played and opposite role and attenuated the effects of MORT overexpression.
conclusionTherefore, lncRNA MORT is upregulated in myocardial infarction and promotes the apoptosis of cardiomyocyte by downregulating miR-93.
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