程序性坏死：缺血再灌注损伤中的新靶点

程序性坏死是新发现的一种细胞死亡方式，在凋亡通路抑制条件下，死亡受体与配体结合可调控非半胱氨酸天冬氨酸蛋白酶依赖的程序性细胞死亡，具备典型的坏死样形态学特征，可触发显著的炎症反应。含死亡域的受体相互作用蛋白激酶1/3在程序性坏死的调节中发挥特异性激酶作用，且可被坏死性抑制剂特异性抑制。程序性坏死在缺血再灌注损伤中的重要作用备受关注，研究已发现其在心、肾、脑组织及视网膜等缺血再灌注损伤中可作为细胞死亡的主要形式。

Programmed necrosis: a new target for#br# ischemia reperfusion injury

Recent years, the researchers have found a new type of cell death, referred to programmed necrosis or necroptosis, which involves the death receptor and the ligand binds and is initiated under the inhibition of apoptosis pathway. Programmed necrosis possesses the morphological features of typical necrosis accompanied by inflammation. The receptor interacting protein kinase 1/3(RIPK1/3) can be inhibited by the specific inhibitors, such as necrostatin-1. RIPK1/3 could regulate programmed necrosis and play a key role in the process. The significance of programmed necrosis in ischemia-reperfusion injury (IRI) has been attracted great attention at present. Simultaneously, a series of studies have found it also involves in the IRI of heart, kidney, brain and retina.