下调和上调
医学
体温过低
心肌梗塞
心功能曲线
长非编码RNA
心脏病学
缺血
内科学
药理学
心力衰竭
生物
基因
生物化学
作者
Jian Zhang,Liming Yu,Yiquan Xu,Yu Liu,Zhi Li,Xiaodong Xue,Song Wan,Huishan Wang
标识
DOI:10.1016/j.ijcard.2017.12.097
摘要
Background Myocardial infarction (MI) is one of the most common causes of cardiac morbidity and mortality. Many evidences suggest that hypothermia have a more pronounced impact as an adjunctive therapy for MI to reduce infarct size. However, the function of long non-coding RNAs (lncRNA) in therapeutic hypothermia for MI remains poorly understood. Methods In this study, we investigated the expression of lncRNA-UIHTC (upregulated in hypothermia treated cardiomyocytes, NONHSAT094064) in ischemic heart tissues. To investigate its function, overexpression of UIHTC was performed by adeno-associated virus vectors after MI model in rat. Results lncRNA-UIHTC was upregulated in ischemic or injury cardiomyocytes. Overexpression of lncRNA-UIHTC in peri-infarction attenuated cardiac dysfunction in vivo. Mechanistically, lncRNA-UIHTC enhanced the mitochondrial function via upregulation of PGC1α. Moreover, when we knocked down PGC1α, the mitochondrial maximal oxygen consumption and ATP levels enhanced by overexpression of UIHTC were nearly completely restored. Conclusions Altogether we have provided a new mechanism whereby hypothermia protected heart against ischemic via lncRNA-UIHTC. The UIHTC provided a new potential therapeutic target for MI but prevented the complications of hypothermia.
科研通智能强力驱动
Strongly Powered by AbleSci AI