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Herbal Munziq Ameliorates Myocardial Ischemia-Reperfusion Injury by Inhibiting Inflammation
Published on: January 10, 2025
MicroRNA-98 attenuates cardiac ischemia-reperfusion injury through inhibiting DAPK1 expression
Chang-Lin Zhai1,2, Guan-Min Tang2, Gang Qian2
1Department of Cardiovascular Diseases, Xinhua Hospital, Shanghai Jiaotong University, School of Medicine, Shanghai, People's Republic of China.
Abstract:
Cardiovascular ischemic disease is a large class of diseases that are harmful to human health. The significant role of microRNAs (miRNAs) in terms of controlling cardiac injury has been reported in latest studies. MiR-98 is very important in regulating the apoptosis, the differentiation, the growth as well as the metastasis of cells. Nevertheless, the effect of miR-98 in the cardiac ischemia reperfusion (I/R) injury has rarely been investigated. In the current research, we found that the miR-98 expression was down-regulated in the cardiomyocytes subjected to hypoxia/reoxygenation (H/R) and in the myocardium of the I/R rats. In addition, over-expression of miR-98 could significantly reduce the myocardial oxidative stress and ischemic injury as well as cell apoptosis. In agreement, similar findings were demonstrated in H9c2 cells subjected to H/R injury. Bioinformatic analysis using MiRanda and TargetScan and luciferase activity assay confirmed death-associated protein kinase 1 (DAPK1) as a direct target of miR-98. These findings suggest that miR-98 may be exploited as a novel molecular marker or therapeutic target for myocardial I/R injury. © 2018 IUBMB Life, 71(1):166-176, 2019.
Insights
MicroRNA-98 (miR-98) is down-regulated in cardiac ischemia reperfusion injury. Increasing miR-98 levels protects against heart damage and cell death, suggesting its therapeutic potential.
Area of Science:
- Cardiovascular Biology
- Molecular Medicine
- Biochemistry
Background:
- Cardiovascular ischemic diseases pose significant health risks.
- MicroRNAs (miRNAs) play a crucial role in regulating cardiac injury.
- The specific role of miR-98 in cardiac ischemia reperfusion (I/R) injury remains largely unexplored.
Purpose of the Study:
- To investigate the expression and function of miR-98 in myocardial ischemia reperfusion (I/R) injury.
- To determine the therapeutic potential of miR-98 in mitigating cardiac I/R damage.
Main Methods:
- Assessed miR-98 expression in cardiomyocytes subjected to hypoxia/reoxygenation (H/R) and in I/R rat myocardium.
- Utilized H9c2 cells to study the effects of miR-98 over-expression on H/R injury.
- Employed bioinformatic analysis (MiRanda, TargetScan) and luciferase assays to identify miR-98 targets.
Main Results:
- miR-98 expression was significantly down-regulated in both H/R cardiomyocytes and I/R rat myocardium.
- Over-expression of miR-98 reduced myocardial oxidative stress, ischemic injury, and apoptosis in H/R-treated H9c2 cells.
- Death-associated protein kinase 1 (DAPK1) was confirmed as a direct target of miR-98.
Conclusions:
- miR-98 expression is decreased during cardiac ischemia reperfusion injury.
- miR-98 exhibits protective effects against myocardial I/R injury by reducing oxidative stress and apoptosis.
- miR-98 presents a potential novel molecular marker and therapeutic target for myocardial I/R injury.
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