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，血流恢复到受伤的心肌本身也会造成损伤，称为缺血再灌注损伤（IRI）。远程缺血调节（RIC）描述了一种现象，即短暂的闭塞和恢复血液流向远离心脏的身体组织，可以保护心肌免受IRI。然而，尽管实验研究取得了可喜的结果，但其作用机制仍然难以捉摸。最近的注意力转向了一种叫做基质细胞衍生因子1 （SDF-1）的小蛋白质，它被认为具有双重功能。首先，SDF-1被认为激活了一种先前与RIC有关的保护机制，即再灌注损伤挽救激酶（RISK）途径。其次，它被认为在吸引干细胞到损伤部位中起作用。因此，SDF-1既可以保护心肌免受IRI，又可以帮助损伤后的心肌修复，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在SDF-1存在的情况下心肌是否可以免受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.