急性心肌梗死（AMI）是最常见致死原因的心血管疾病之一。心梗后心肌细胞缺血缺氧，诱导细胞衰老，导致心室重构，心功能下降，影响预后。本研究发现AMI患者血浆外泌体UCA1升高，并和血浆GDF15成正比；体外实验在证实人间充质干细胞（hMSCs）在缺氧诱导下分泌的外泌体UCA1升高并可抑制心肌细胞衰老的基础上，提出 “hMSCs外泌体UCA1通过调控GDF15抑制心肌细胞衰老” 的假说。拟进一步构建基于UCA1的深度学习预测模型对AMI进行危险分层；采用基因过表达/沉默技术，探讨外泌体介导的UCA1对心肌细胞衰老的作用；通过挽救实验论证UCA1调控GDF15抑制心肌细胞衰老的分子机制；通过RIP、ChIRP等手段研究UCA1的下游分子作用网络；通过以上实验阐明外泌体介导的UCA1抑制心肌细胞衰老的功能、分子机制及其在AMI危险分层中的价值，为治疗AMI提供新思路。

Acute myocardial infarction (AMI) is one of the most common causes of death. Myocardial ischemia and hypoxia induce cell aging, lead to ventricular remodeling and cardiac function decline. Our previous study found that UCA1 increased in plasma exosome of AMI patients and was proportional to GDF15 in plasma. UCA1 increased in exosome secreted by human mesenchymal stem cells (hMSCs) under hypoxia treatment and inhibited myocardial cell senescence. Thus, we put forward hypothesis of “UCA1 of hMSCs exosome inhibited myocardial cell senescence by regulating GDF15”. We intend to further construct UCA1-based deep learning prediction model for risk stratification of AMI; explore the effect of exosome-mediated UCA1 on myocardial cell aging by gene overexpression/silencing technology; demonstrate the molecular mechanism of UCA1 regulating GDF15 inhibiting myocardial cell aging; and study the downstream molecular network of UCA1 by RIP and ChIRP. Our study will clarify the function and molecular mechanism of exosome UCA1 in inhibiting myocardial cell senescence and its value in risk stratification of AMI, and provide new ideas for the treatment of AMI.