Cardiovascular Research Chair, UAB, Barcelona, Spain.
CIBER-CV, Instituto de Salud Carlos III, Madrid, Spain.
Curr Pharm Des. 2018;24(25):2967-2973. doi: 10.2174/1381612824666180629162726.
Advances in early reperfusion therapies focused on the revascularization of the ischemic tissues, in the last decades, lead to reduced mortality in acute myocardial infarction (MI) patients. However, a large proportion of patients show inadequate myocardial perfusion because of dysfunction of the microcirculation. The high prevalence of microvascular dysfunction after reperfusion therapies and the negative prognostic of this procedure justify the search for therapeutic strategies that aim to restore the microvascular network. It is well known that the size of the initial infarct, the duration of ischemia and the efficiency of reperfusion determine myocardial tissue damage and cardiomyocyte loss after myocardial infarction. Therefore any advancement on the mechanisms that induce the repair process of microvascular dysfunction after reperfused MI is of great interest. Here, we will review the different proteins and cells known to participate in angiogenesis induction post-MI and we will also discuss the potential pharmacological and cellular processes that promote the recovery of microvasculature by angiogenesis stimulation after MI.
在过去几十年中，针对缺血组织再灌注的早期治疗方法的进展，降低了急性心肌梗死（MI）患者的死亡率。然而，由于微循环功能障碍，很大一部分患者的心肌灌注不足。再灌注治疗后微血管功能障碍的高患病率以及该治疗程序的不良预后，证明有必要寻找旨在恢复微血管网络的治疗策略。众所周知，初始梗死的大小、缺血的持续时间和再灌注的效率决定了心肌梗死后心肌组织损伤和心肌细胞的丧失。因此，任何关于导致再灌注后 MI 中小血管功能障碍修复过程的机制的进展都具有重要意义。在这里，我们将回顾已知参与 MI 后血管生成诱导的不同蛋白质和细胞，我们还将讨论通过 MI 后血管生成刺激促进微血管恢复的潜在药理学和细胞过程。
