自噬
声动力疗法
细胞凋亡
心肌梗塞
心力衰竭
医学
活性氧
缺氧(环境)
心功能曲线
内科学
细胞生物学
心脏病学
癌症研究
化学
生物
生物化学
氧气
有机化学
作者
Yingjie Xu,Zengxiang Dong,Rongzhen Zhang,Zeng Wang,Yuanqi Shi,Mingyu Li,Jiemei Yang,Tao Yang,Runtong Zhang,Tengyu Wang,Jingyu Zhang,Yu Zhang,Xiang Fei,Yu Han,Jiawen Wu,Zhihan Miao,Qiuyu Chen,Qi Li,Zeyao Wang,Ye Tian,Yuanyuan Guo
标识
DOI:10.1016/j.freeradbiomed.2022.12.080
摘要
Myocardial infarction (MI) is lethal to patients because of acute ischemia and hypoxia leading to cardiac tissue apoptosis. Autophagy played a key role in MI through affecting the survival of cardiomyocytes. LncRNA-MHRT (myosin heavy-chain-associated RNA transcripts) was specific to the heart and cardiomyocytes, and inhibition of lncRNA-MHRT transcription under pathological stimuli could cause cardiac hypertrophy and even heart failure (HF). Sonodynamic therapy (SDT) is a new and developing medical technique that utilizes low-intensity ultrasound to locally activate a preloaded sonosensitizer. Our group previously reported that SDT could regulate autophagy. In this study, we investigated whether SDT could reduce MI-induced cardiomyocyte apoptosis via activating autophagy pathway. SDT improved cardiac function and suppresses MI-induced cardiomyocyte apoptosis. SDT alleviated MI-induced cardiomyocyte apoptosis by improving autophagy. MHRT mediated the inhibiting effect of SDT on cardiomyocyte apoptosis via activating autophagy pathway. Our data reveal a novel effect that SDT protects against MI and confirm that SDT reduces MI-induced cardiomyocyte apoptosis via activating MHRT-mediated-autophagy. Thus, our findings also indicate that SDT may be used as a potential method for treatment of post-myocardial infarction heart failure.
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