Oxidative stress and endoplasmic reticulum (ER) stress in the development of neonatal hypoxic-ischaemic brain injury

被引：64

作者：

Thornton, Claire ^{[1
]}

Baburamani, Ana A. ^{[1
]}

Kichev, Anton ^{[1
]}

Hagberg, Henrik ^{[1
,2
]}

机构：

[1] Kings Coll London, Kings Hlth Partners, St Thomas Hosp, Perinatal Brain Injury Grp,Ctr Developing Brain,D, London SE1 7EH, England

[2] Univ Gothenburg, Sahlgrenska Acad, Inst Clin Sci & Physiol & Neurosci, Perinatal Ctr, S-41685 Gothenburg, Sweden

来源：

BIOCHEMICAL SOCIETY TRANSACTIONS | 2017年 / 45卷

基金：

英国惠康基金; 英国医学研究理事会; 瑞典研究理事会;

关键词：

NITRIC-OXIDE SYNTHASE; UNFOLDED PROTEIN RESPONSE; POSTRESUSCITATION N-ACETYLCYSTEINE; DISMUTASE TRANSGENIC MICE; ELECTRON-TRANSPORT CHAIN; UMBILICAL-CORD OCCLUSION; CELL-DEATH; REACTIVE OXYGEN; RAT-BRAIN; MITOCHONDRIAL DYSFUNCTION;

D O I：

10.1042/BST20170017

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

Birth asphyxia in term neonates affects 1-2/1000 live births and results in the development of hypoxic-ischaemic encephalopathy with devastating life-long consequences. The majority of neuronal cell death occurs with a delay, providing the potential of a treatment window within which to act. Currently, treatment options are limited to therapeutic hypothermia which is not universally successful. To identify new interventions, we need to understand the molecular mechanisms underlying the injury. Here, we provide an overview of the contribution of both oxidative stress and endoplasmic reticulum stress in the development of neonatal brain injury and identify current preclinical therapeutic strategies.

引用

页码：1067 / 1076

页数：10

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