Abstract
The universe of painful Na-channelopathies--human disorders caused by mutations in voltage-gated sodium channels--has recently expanded in three dimensions. We now know that mutations of sodium channels cause not only rare genetic 'model disorders' such as inherited erythromelalgia and channelopathy-associated insensitivity to pain but also common painful neuropathies. We have learned that mutations of NaV1.8, as well as mutations of NaV1.7, can cause painful Na-channelopathies. Moreover, recent studies combining atomic level structural models and pharmacogenomics suggest that the goal of genomically guided pain therapy may not be unrealistic.
Copyright © 2013 Elsevier Ltd. All rights reserved.
MeSH terms
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Animals
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Channelopathies / drug therapy
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Channelopathies / genetics*
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Erythromelalgia / drug therapy
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Erythromelalgia / genetics
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Gene Expression Regulation
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Genetic Association Studies
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Humans
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Mutation
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NAV1.7 Voltage-Gated Sodium Channel / genetics
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NAV1.8 Voltage-Gated Sodium Channel / genetics
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Pain / drug therapy
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Pain / genetics*
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Pain Threshold
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Peripheral Nervous System Diseases / drug therapy
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Peripheral Nervous System Diseases / genetics*
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Pharmacogenetics
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Rectum / abnormalities
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Rectum / drug effects
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Sodium Channels / genetics*
Substances
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NAV1.7 Voltage-Gated Sodium Channel
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NAV1.8 Voltage-Gated Sodium Channel
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Sodium Channels
Supplementary concepts
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Neuropathy, Painful
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Paroxysmal Extreme Pain Disorder