Neuroglobin, a Novel Target for Endogenous Neuroprotection against Stroke and Neurodegenerative Disorders

International Journal of Molecular Sciences

Zhanyang Yu²  Ning Liu²  Jianxiang Liu¹  Kevin Yang² 

[1] National Institute for Radiological Protection, China Center for Disease Control and Prevention, Beijing 100088, China; E-Mail:;Neuroprotection Research Laboratory, Department of Neurology and Radiology, Massachusetts General Hospital, Neuroscience Program, Harvard Medical School, Room 2401/2411A, 149 13th Street, Charlestown Boston, MA 02129, USA; E-Mails:

关键词: neuroglobin;    neuroprotection;    stroke;    neurodegenerative diseases;    hypoxia/ischemia;    high-throughput screening;   

DOI  :  10.3390/ijms13066995

来源: mdpi

【 摘 要 】

Brain neurons and tissues respond to sublethal injury by activating endogenous protective pathways. Recently, following the failure of a large number of clinical trials for protective strategies against stroke that aim to inhibit a specific ischemia response pathway, endogenous neuroprotection has emerged as a more promising and hopeful strategy for development of therapeutics against stroke and neurodegenerative disorders. Neuroglobin (Ngb) is an oxygen-binding globin protein that is highly and specifically expressed in brain neurons. Accumulating evidence have clearly demonstrated that Ngb is an endogenous neuroprotective molecule against hypoxic/ischemic and oxidative stress-related insults in cultured neurons and animals, as well as neurodegenerative disorders such as Alzheimer’s disease, thus any pharmacological strategy that can up-regulate endogenous Ngb expression may lead to novel therapeutics against these brain disorders. In this review, we summarize recent studies about the biological function, regulation of gene expression, and neuroprotective mechanisms of Ngb. Furthermore, strategies for identification of chemical compounds that can up-regulate endogenous Ngb expression for neuroprotection against stroke and neurodegenerative disorders are discussed.

【 授权许可】

CC BY   
© 2012 by the authors; licensee Molecular Diversity Preservation International, Basel, Switzerland.