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Neuronal death after perinatal cerebral hypoxia‐ischemia: Focus on autophagy—mediated cell death
Author(s) -
Descloux C.,
Ginet V.,
Clarke P.G.H.,
Puyal J.,
Truttmann A.C.
Publication year - 2015
Publication title -
international journal of developmental neuroscience
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.761
H-Index - 88
eISSN - 1873-474X
pISSN - 0736-5748
DOI - 10.1016/j.ijdevneu.2015.06.008
Subject(s) - hypoxia (environmental) , autophagy , programmed cell death , neuroprotection , ischemia , medicine , encephalopathy , neuroscience , apoptosis , hypoxic ischemic encephalopathy , cerebral hypoxia , stroke (engine) , biology , mechanical engineering , biochemistry , chemistry , organic chemistry , oxygen , engineering
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.