The potential importance of Stromal Derived Factor-1 in the protection and repair of myocardium following simulated ischaemia-reperfusion injury

心脏病发作后，受损心肌的血流量恢复本身就会造成损伤，称为缺血再灌注损伤(IRI)。远程缺血适应(RIC)描述的现象是短暂阻断和恢复流向远离心脏的身体组织的血液可以保护心肌免受IRI的影响。然而，尽管实验研究取得了令人振奋的结果，但其作用机制仍然难以捉摸。最近，人们的注意力转向了一种名为基质细胞衍生因子1(SDF-1)的小蛋白，它被认为具有双重功能。首先，SDF-1被认为激活了先前在RIC中所涉及的保护机制，即再灌注损伤挽救激酶(RISK)途径。其次，它被认为在将干细胞吸引到损伤部位方面发挥了作用。因此，SDF-1既保护心肌免受IRI，又有助于损伤后的修复，从而减少心力衰竭是可行的。我研究的主要目标是在动物模型中证明SDF-1是否可以保护心肌免受IRI的影响，并确定SDF-1在预防心力衰竭方面的益处。

Following a heart attack, the restoration of blood flow to injured heart muscle can itself inflict injury, known as Ischaemia-Reperfusion Injury (IRI). Remote Ischaemic Conditioning (RIC) describes the phenomenon whereby the brief occlusion and restoration of blood flow to body tissues remote from the heart can protect heart muscle from IRI. However, despite promising results from experimental studies, the mechanism of action remains elusive. Recent attention has turned to a small protein called Stromal Cell-Derived Factor 1 (SDF-1), which is thought to have a dual function. Firstly, SDF-1 is thought to activate a protective mechanism that has previously been implicated in RIC, namely the Reperfusion Injury Salvage Kinase (RISK) pathway. Secondly, it is thought to play a role in attracting stem cells to the site of injury. It is therefore feasible that SDF-1 both protects heart muscle from IRI and helps repair it after injury, thus reducing heart failure. The key goals of my research are to demonstrate whether heart muscle can be protected from IRI in the presence of SDF-1 in animal models, and to ascertain the benefit of SDF-1 in preventing heart failure.