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Published on: January 10, 2025
Inhibiting miR-205 Alleviates Cardiac Ischemia/Reperfusion Injury by Regulating Oxidative Stress, Mitochondrial
Yuerong Xu1,2, Wangang Guo1, Di Zeng1
1Department of Cardiology, Tangdu Hospital, The Fourth Military Medical University, Xi'an, China.
Background:
miR-205 is important for oxidative stress, mitochondrial dysfunction, and apoptosis. The roles of miR-205 in cardiac ischemia/reperfusion (I/R) injury remain unknown. The aim of this research is to reveal whether miR-205 could regulate cardiac I/R injury by focusing upon the oxidative stress, mitochondrial function, and apoptosis.
Methods:
Levels of miR-205 and Rnd3 were examined in the hearts with I/R injury. Myocardial infarct size, cardiac function, oxidative stress, mitochondria function, and cardiomyocyte apoptosis were detected in mice with myocardial ischemia/reperfusion (MI/R) injury. The primary neonatal cardiomyocytes underwent hypoxia/reoxygenation (H/R) to simulate MI/R injury.
Results:
miR-205 levels were significantly elevated in cardiac tissues from I/R in comparison with those from Sham. In comparison with controls, levels of Rnd3 were significantly decreased in the hearts from mice with MI/R injury. Furthermore, inhibiting miR-205 alleviated MI/R-induced apoptosis, reduced infarct size, prevented oxidative stress increase and mitochondrial fragmentation, and improved mitochondrial functional capacity and cardiac function. Consistently, overexpression of miR-205 increased infarct size and promoted apoptosis, oxidative stress, and mitochondrial dysfunction in mice with MI/R injury. In cultured mouse neonatal cardiomyocytes, downregulation of miR-205 reduced oxidative stress in H/R-treated cardiomyocytes. Finally, inhibiting Rnd3 ablated the cardioprotective effects of miR-205 inhibitor in MI/R injury.
Conclusions:
We conclude that inhibiting miR-205 reduces infarct size, improves cardiac function, and suppresses oxidative stress, mitochondrial dysfunction, and apoptosis by promoting Rnd3 in MI/R injury. miR-205 inhibitor-induced Rnd3 activation is a valid target to treat MI/R injury.
Insights
Inhibiting miR-205 protects the heart from ischemia/reperfusion injury by reducing apoptosis and oxidative stress. This protection is mediated by Rnd3, offering a potential therapeutic target for cardiac injury.
Area of Science:
- Cardiovascular Research
- Molecular Biology
- Cellular Biology
Background:
- MicroRNA-205 (miR-205) plays a role in oxidative stress, mitochondrial dysfunction, and apoptosis.
- The specific involvement of miR-205 in cardiac ischemia/reperfusion (I/R) injury is not well understood.
Purpose of the Study:
- To investigate the regulatory role of miR-205 in cardiac I/R injury.
- To elucidate the mechanisms involving oxidative stress, mitochondrial function, and apoptosis.
Main Methods:
- Examined miR-205 and Rnd3 levels in I/R cardiac tissues.
- Assessed myocardial infarct size, cardiac function, oxidative stress, mitochondrial function, and apoptosis in a mouse model of myocardial ischemia/reperfusion (MI/R) injury.
- Utilized hypoxia/reoxygenation (H/R) in primary neonatal cardiomyocytes to simulate MI/R injury.
Main Results:
- miR-205 levels were elevated, while Rnd3 levels were decreased in I/R cardiac tissues.
- Inhibiting miR-205 reduced infarct size, apoptosis, oxidative stress, and mitochondrial dysfunction, while improving cardiac function.
- Overexpression of miR-205 exacerbated MI/R injury.
- Downregulation of miR-205 reduced oxidative stress in H/R-treated cardiomyocytes.
- Inhibiting Rnd3 abolished the protective effects of miR-205 inhibition.
Conclusions:
- Inhibiting miR-205 mitigates cardiac I/R injury by enhancing Rnd3, thereby suppressing oxidative stress, mitochondrial dysfunction, and apoptosis.
- Targeting miR-205 inhibition and subsequent Rnd3 activation presents a viable therapeutic strategy for treating MI/R injury.
