Abstract
Hypoxia inducible factor-1 (HIF-1) is a transcriptional factor responsible for cellular and tissue adaption to low oxygen tension. HIF-1, a heterodimer consisting of a constitutively expressed β subunit and an oxygen-regulated α subunit, regulates a series of genes that participate in angiogenesis, iron metabolism, glucose metabolism, and cell proliferation/survival. The activity of HIF-1 is controlled by post-translational modifications on different amino acid residues of its subunits, mainly the alpha subunit. Besides in ischemic stroke (see review [1]), emerging evidence has revealed that HIF-1 activity and expression of its down-stream genes, such as vascular endothelial growth factor and erythropoietin, are altered in a range of neurodegenerative diseases. At the same time, experimental and clinical evidence has demonstrated that regulating HIF-1 might ameliorate the cellular and tissue damage in the neurodegenerative diseases. These new findings suggest HIF-1 as a potential medicinal target for the neurodegenerative diseases. This review focuses on HIF-1α protein modifications and HIF-1's potential neuroprotective roles in Alzheimer's (AD), Parkinson's (PD), Huntington's diseases (HD), and amyotrophic lateral sclerosis (ALS).
Keywords: AD, ALS, EPO, HD, HIF-1, PD, VEGF, protein modification, prolyl hydroxylase inhbitor, iron chelator, 2-oxoglutarate analogues, cobalt
Current Medicinal Chemistry
Title: Hypoxia Inducible Factor-1 as a Target for Neurodegenerative Diseases
Volume: 18 Issue: 28
Author(s): Z. Zhang, J. Yan, Y. Chang, S. ShiDu Yan and H. Shi
Affiliation:
Keywords: AD, ALS, EPO, HD, HIF-1, PD, VEGF, protein modification, prolyl hydroxylase inhbitor, iron chelator, 2-oxoglutarate analogues, cobalt
Abstract: Hypoxia inducible factor-1 (HIF-1) is a transcriptional factor responsible for cellular and tissue adaption to low oxygen tension. HIF-1, a heterodimer consisting of a constitutively expressed β subunit and an oxygen-regulated α subunit, regulates a series of genes that participate in angiogenesis, iron metabolism, glucose metabolism, and cell proliferation/survival. The activity of HIF-1 is controlled by post-translational modifications on different amino acid residues of its subunits, mainly the alpha subunit. Besides in ischemic stroke (see review [1]), emerging evidence has revealed that HIF-1 activity and expression of its down-stream genes, such as vascular endothelial growth factor and erythropoietin, are altered in a range of neurodegenerative diseases. At the same time, experimental and clinical evidence has demonstrated that regulating HIF-1 might ameliorate the cellular and tissue damage in the neurodegenerative diseases. These new findings suggest HIF-1 as a potential medicinal target for the neurodegenerative diseases. This review focuses on HIF-1α protein modifications and HIF-1's potential neuroprotective roles in Alzheimer's (AD), Parkinson's (PD), Huntington's diseases (HD), and amyotrophic lateral sclerosis (ALS).
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Cite this article as:
Zhang Z., Yan J., Chang Y., ShiDu Yan S. and Shi H., Hypoxia Inducible Factor-1 as a Target for Neurodegenerative Diseases, Current Medicinal Chemistry 2011; 18 (28) . https://dx.doi.org/10.2174/092986711797200426
DOI https://dx.doi.org/10.2174/092986711797200426 |
Print ISSN 0929-8673 |
Publisher Name Bentham Science Publisher |
Online ISSN 1875-533X |
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