Descloux C, Ginet V, Clarke P G H, Puyal J, Truttmann A C
Department of Fundamental Neurosciences (DNF), University of Lausanne, Rue du Bugnon 9, 1005 Lausanne, Switzerland; Clinic of Neonatology, Department of Pediatrics and Pediatric Surgery, University Hospital Center and University of Lausanne, 1011 Lausanne, Vaud, Switzerland.
Department of Fundamental Neurosciences (DNF), University of Lausanne, Rue du Bugnon 9, 1005 Lausanne, Switzerland.
Int J Dev Neurosci. 2015 Oct;45:75-85. doi: 10.1016/j.ijdevneu.2015.06.008. Epub 2015 Jul 28.
Neonatal hypoxic-ischemic encephalopathy is a critical cerebral event occurring around birth with high mortality and neurological morbidity associated with long-term invalidating sequelae. In view of the great clinical importance of this condition and the lack of very efficacious neuroprotective strategies, it is urgent to better understand the different cell death mechanisms involved with the ultimate aim of developing new therapeutic approaches. The morphological features of three different cell death types can be observed in models of perinatal cerebral hypoxia-ischemia: necrotic, apoptotic and autophagic cell death. They may be combined in the same dying neuron. In the present review, we discuss the different cell death mechanisms involved in neonatal cerebral hypoxia-ischemia with a special focus on how autophagy may be involved in neuronal death, based: (1) on experimental models of perinatal hypoxia-ischemia and stroke, and (2) on the brains of human neonates who suffered from neonatal hypoxia-ischemia.
新生儿缺氧缺血性脑病是一种发生在出生前后的严重脑部事件，死亡率高，且会导致具有长期致残后遗症的神经功能障碍。鉴于这种疾病具有重大的临床意义，且缺乏非常有效的神经保护策略，迫切需要更好地了解所涉及的不同细胞死亡机制，最终目的是开发新的治疗方法。在围产期脑缺氧缺血模型中可以观察到三种不同细胞死亡类型的形态学特征：坏死性、凋亡性和自噬性细胞死亡。它们可能存在于同一个濒死神经元中。在本综述中，我们将讨论新生儿脑缺氧缺血所涉及的不同细胞死亡机制，特别关注自噬如何可能参与神经元死亡，其依据为：（1）围产期缺氧缺血和中风的实验模型，以及（2）患有新生儿缺氧缺血的人类新生儿的大脑。
