慢性缺氧类心脏病患者可能需要体外循环下手术治疗，其预后与术中心肌保护相关。研究表明远端缺血预处理（RIPC）在缺血再灌注中有心肌保护作用。目前，RIPC发挥心肌保护作用存在争议且具体机制不明确。前期研究发现RIPC增高法四患者pSTAT3、HIF-1α蛋白水平，改善线粒体结构，发挥保护作用。据此提出假说：RIPC活化STAT3、稳定HIF-1α并促进其转录，增加frataxin，抑制mPTP的开放，最终保护心肌。本课题将从慢性缺氧角度探讨STAT3/HIF-1α /frataxin轴介导RIPC在慢性缺氧心肌线粒体的保护作用机制。项目拟建立慢性缺氧模型，从分子、细胞及动物等水平研究RIPC在慢性缺氧心肌保护作用机制，为慢性缺氧患者接受心脏手术时采取RIPC提供确切理论依据；寻找RIPC在慢性缺氧患者心肌保护作用的治疗靶点，为慢性缺氧患者行心脏手术时心肌缺血再灌注损伤提供新的实施预防措施。

Patients with chronic hypoxic cardiopathy such as coronary heart disease and tetralogy of Fallot (TOF) may require surgery under cardiopulmonary bypass (CPB) anesthesia. Many researches indicate that the remote ischemic preconditioning has the myocardial protective effect in CPB ischemia reperfusion, however, there is still controversy. At present, the specific mechanism of the myocardium protection of RIPC is not clear. Our previous study found that the perioperative RIPC of TOF patients could lead to increased levels of STAT3 and Hif-1α in myocardium, and improved mitochondrial structure. Therefore, we hypothesize that RIPC can activate pSTAT3, stabilize Hif-1α protein and promote its transcription to increase Hif-1α, increase frataxin expression, which ultimately regulate mitochondrial function and inhibit mitochondrial mPTP opening. This research will performed in vitro and in vivo, clear STAT3 / HIF - 1α/frataxin mediated myocardial mitochondria protection in chronic hypoxia.This research will clarify the myocardial protection mechanism of STAT3 / HIF - 1α/frataxin, and provide a theoretical basis for the subsequent clinical extension application.