心肌缺血再灌注损伤的防治是临床面临的难题和挑战，亟需加强其机制研究，发现新的干预靶点。lncRNA（long noncoding RNA）是一类重要新型调控分子，参与疾病过程的调控。本研究的目的是探讨lncRNA-072211对心脏缺血再灌注损伤的作用和机制。我们前期研究发现：1）lncRNA-072211在缺血心肌组织升高近2倍，在心肌细胞损伤模型中升高1倍；2）过表达lncRNA-072211加重缺血心脏功能和心肌细胞凋亡，而沉默其表达能够改善心脏功能和抑制心肌细胞凋亡；3）RNA pull down结合质谱分析发现lncRNA-072211与ERC1蛋白相结合形成RNA-蛋白复合体；4）敲减ERC1能够加重过氧化氢诱导的心肌细胞损伤。因此，我们假设：lncRNA-072211与ERC1结合通过细胞凋亡通路调控心肌缺血再灌注损伤，阐明其在缺血再灌注损伤中的作用与分子调控机制。

The prevention and treatment of myocardial ischemia-reperfusion injury is a challenging problem. To understand its mechanism and discover novel target is in urgent need. LncRNAs (long noncoding RNAs) are a new class of regulatory molecules and participate in the regulation of the disease process. The aim of this study is to investigate the effects and underlying mechanisms of lncRNA-072211 on cardiac ischemia-reperfusion injury. Our previous results showed that: 1) lncRNA-072211 was upregulated about 2-fold in myocardial ischemia and 1-fold in myocardial cell injury model; 2) overexpression of lncRNA-072211 aggravated cardiac function in the ischemic heart and myocardial cell apoptosis, and its silencing improved cardiac function and attenuated the apoptosis of myocardial cells; 3) mass spectrometry analyses of RNA pull down showed that lncRNA-072211 could be combined with ERC1 protein to form RNA- protein complex; 4) knockdown of ERC1 aggravated myocardial cell injury induced by H2O2. Therefore, we hypothesized that the interaction of lncRNA-072211 and ERC1 regulates myocardial ischemia-reperfusion injury through regulating apoptosis pathway, which elucidates the functions and molecular mechanism of lncRNA-072211 in ischemia-reperfusion injury.