Molecular chaperones and hypoxic-ischemic encephalopathy

被引:1
作者
Cong Hua [1 ]
Wei-na Ju [2 ]
Hang Jin [2 ]
Xin Sun [2 ]
Gang Zhao [1 ]
机构
[1] Department of Neurosurgery,The First Hospital of Jilin University
[2] Department of Neurology,The First Hospital of Jilin University
关键词
nerve regeneration; hypoxic-ischemic encephalopathy; molecular chaperones; excitatory amino acid; cellular proteolysis; oxygen radicals; inflammation; apoptosis; reviews; neural regeneration;
D O I
暂无
中图分类号
R743.3 [急性脑血管疾病(中风)];
学科分类号
1002 ;
摘要
Hypoxic-ischemic encephalopathy(HIE) is a disease that occurs when the brain is subjected to hypoxia,resulting in neuronal death and neurological deficits,with a poor prognosis.The mechanisms underlying hypoxic-ischemic brain injury include excitatory amino acid release,cellular proteolysis,reactive oxygen species generation,nitric oxide synthesis,and inflammation.The molecular and cellular changes in HIE include protein misfolding,aggregation,and destruction of organelles.The apoptotic pathways activated by ischemia and hypoxia include the mitochondrial pathway,the extrinsic Fas receptor pathway,and the endoplasmic reticulum stress-induced pathway.Numerous treatments for hypoxic-ischemic brain injury caused by HIE have been developed over the last half century.Hypothermia,xenon gas treatment,the use of melatonin and erythropoietin,and hypoxic-ischemic preconditioning have proven effective in HIE patients.Molecular chaperones are proteins ubiquitously present in both prokaryotes and eukaryotes.A large number of molecular chaperones are induced after brain ischemia and hypoxia,among which the heat shock proteins are the most important.Heat shock proteins not only maintain protein homeostasis; they also exert anti-apoptotic effects.Heat shock proteins maintain protein homeostasis by helping to transport proteins to their target destinations,assisting in the proper folding of newly synthesized polypeptides,regulating the degradation of misfolded proteins,inhibiting the aggregation of proteins,and by controlling the refolding of misfolded proteins.In addition,heat shock proteins exert anti-apoptotic effects by interacting with various signaling pathways to block the activation of downstream effectors in numerous apoptotic pathways,including the intrinsic pathway,the endoplasmic reticulum-stress mediated pathway and the extrinsic Fas receptor pathway.Molecular chaperones play a key role in neuroprotection in HIE.In this review,we provide an overview of the mechanisms of HIE and discuss the various treatment strategies.Given their critical role in the disease,molecular chaperones are promising therapeutic targets for HIE.
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页码:153 / 160
页数:8
相关论文
共 38 条
  • [1] Transplantation of vascular endothelial growth factor-modified neural stem/progenitor cells promotes the recovery of neurological function following hypoxic-ischemic brain damage[J]. Yue Yao,Xiang-rong Zheng,Shan-shan Zhang,Xia Wang,Xiao-he Yu,Jie-lu Tan,Yu-jia Yang.Neural Regeneration Research. 2016(09)
  • [2] Neuroprotective effects of ginsenoside Rg1-induced neural stem cell transplantation on hypoxic-ischemic encephalopathy
    Ying-bo Li
    Yan Wang
    Ji-ping Tang
    Di Chen
    Sha-li Wang
    [J]. Neural Regeneration Research, 2015, 10 (05) : 753 - 759
  • [3] Melatonin influences NO/NOS pathway and reduces oxidative and nitrosative stress in a model of hypoxic-ischemic brain damage[J] . Santos Blanco,Raquel Hernández,Gustavo Franchelli,Manuel Miguel Ramos-álvarez,María ángeles Peinado.Nitric Oxide . 2017
  • [4] Xenon protects left ventricular diastolic function during acute ischemia, less than ischemic preconditioning[J] . Jan Baumert,Anna Roehl,Sandra Funcke,Marc Hein.Medical Gas Research . 2016 (3)
  • [5] Methods for monitoring Ca 2+ and ion channels in the lysosome[J] . Xi Zo? Zhong,Yiming Yang,Xue Sun,Xian-Ping Dong.Cell Calcium . 2016
  • [6] Nitric oxide induces hypoxia ischemic injury in the neonatal brain via the disruption of neuronal iron metabolism[J] . Qing Lu,Valerie A. Harris,Ruslan Rafikov,Xutong Sun,Sanjiv Kumar,Stephen M. Black.Redox Biology . 2015
  • [7] Mechanisms of Neuronal Protection against Excitotoxicity, Endoplasmic Reticulum Stress, and Mitochondrial Dysfunction in Stroke and Neurodegenerative Diseases[J] . Howard Prentice,Jigar Pravinchandra Modi,Jang-Yen Wu,Claudio Cabello-Verrugio.Oxidative Medicine and Cellular Longevity . 2015
  • [8] Therapeutic hypothermia for stroke: Where to go?[J] . Ziping Han,Xiangrong Liu,Yumin Luo,Xunming Ji.Experimental Neurology . 2015
  • [9] The complex contribution of chemokines to neuroinflammation: switching from beneficial to detrimental effects[J] . Ophélia Thuc,Nicolas Blondeau,Jean‐Louis Nahon,Carole Rovère.Ann. N.Y. Acad. Sci. . 2015 (1)
  • [10] Global, regional, and national causes of child mortality in 2000–13, with projections to inform post-2015 priorities: an updated systematic analysis[J] . Li Liu,Shefali Oza,Daniel Hogan,Jamie Perin,Igor Rudan,Joy E Lawn,Simon Cousens,Colin Mathers,Robert E Black.The Lancet . 2015 (9966)