Inhibiting miR-205 Alleviates Cardiac Ischemia/Reperfusion Injury by Regulating Oxidative Stress, Mitochondrial Function, and Apoptosis.
Yuerong XuWangang GuoDi ZengYexian FangRunze WangDong GuoBingchao QiYugang XueFeng XueZuolin JinYan LiMingming ZhangPublished in: Oxidative medicine and cellular longevity (2021)
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.
Keyphrases
- oxidative stress
- ischemia reperfusion injury
- diabetic rats
- cell proliferation
- long non coding rna
- long noncoding rna
- signaling pathway
- induced apoptosis
- dna damage
- endoplasmic reticulum stress
- cell cycle arrest
- heart failure
- left ventricular
- acute coronary syndrome
- percutaneous coronary intervention
- mouse model
- atrial fibrillation