高龄是心肌梗死的危险因素之一，端粒缩短与端粒酶活性下降亦与缺血性心脏病的发生有关。端粒重复序列结合因子2（TRF2）是保护端粒末端的蛋白，表达下降时，会引起端粒缩短，加速细胞衰老。本课题组前期研究发现：正常心肌缺血后处理可以改善缺血再灌注损伤，但是老化心肌的这种保护作用“钝化”，与TRF2、ALKBH5/lncRNA H19表达下降有关。为探究TRF2在老化心肌缺血后处理中的作用及其机制，先向老年小鼠注射TRF2腺相关病毒及其对照进行缺血后处理在体功能实验，在机制方面，我们推测ALKBH5可能通过影响STAT3 mRNA m6A甲基化修饰程度影响其表达，H19亦可能通过miR-124-3p调控STAT3，而STAT3作为转录因子可能通过调控TRF2减轻老化心肌线粒体功能障碍和端粒损伤，减少炎症因子的释放，最终减轻缺血后处理损伤。通过本研究可为老年缺血性心脏病患者提供新的治疗靶点和思路。

Aging is one of the risk factors for myocardial infarction, and shortened telomeres as well as decreased telomerase activity are also associated with ischemic heart disease. Telomere repeat binding factor 2 (TRF2) is a protein that protects telomere terminals. When TRF2 expression decreases, telomere shortening and accelerate cell senescence, but its role in myocardial ischemia/reperfusion (I/R) of elderly patients remains to be investigated. Our previous research identified ischemia postconditioning(I/Post), brief intermittent episodes of I/R at the onset of reperfusion after a prolonged period of ischemia, as a potentially effective method to alleviate I/R injury, but it may not be effective in the aged heart due to the low expressions of TRF2, ALKBH5/lncRNA H19. In order to explore the effect and mechanism of TRF2 in I/Ppost of aged heart, the aged mice were subjected to I/Post following injected TRF2 AAV9 virus and its negative control in vivo. We speculate that STAT3 m6A methylation level and expression could be regulated by ALKBH5, H19 may mediate STAT3 expression by targeting miR-124-3p. TRF2 may be regulated by STAT3, a transcription factor, alleviate mitochondrial dysfunction and telomere damage in senescence cardiomyocytes, reduce the release of inflammatory factors, and moderate I/Post injury ultimately. The research may provide new therapeutic targets and ideas for elderly patients with ischemic heart disease.