Linked Life Data

20146699

Source:http://linkedlifedata.com/resource/pubmed/id/20146699

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:dateCreated
2010-2-11
pubmed:abstractText
The literature currently suggests that voltage-gated sodium channels play a major role in the pathogenesis of neuropathic pain. Alterations in the expression and targeting of specific sodium channels within injured dorsal root ganglia neurons appear to predispose the neurons to abnormal firing properties, allowing for the development of neuropathic pain. Mutations of one particular sodium channel (Na(v)1.7) have been shown to cause inherited neuropathic pain in humans, specifically in erythromelalgia and paroxysmal extreme pain disorder. Inherited erythromelalgia is the first human pain syndrome to be understood at a molecular level, having been linked to gain-of-function mutations of Na(v)1.7. Conversely, a loss-of-function of the Na(v)1.7 channel can produce channelopathy-associated insensitivity to pain. Therefore, the Na(v)1.7 channel may provide a unique target for the pharmacotherapy of pain in humans. In this review article we summarize current knowledge regarding several different disease manifestations arising from changes within the Na(v)1.7 channel.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jan
pubmed:issn
1749-6632
pubmed:author
pubmed:issnType
Electronic
pubmed:volume
1184
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
196-207
pubmed:dateRevised
2010-4-28
pubmed:meshHeading
pubmed:year
2010
pubmed:articleTitle
Familial pain syndromes from mutations of the NaV1.7 sodium channel.
pubmed:affiliation
Department of Neurology, Yale University School of Medicine, New Haven, Connecticut, USA.
pubmed:publicationType
Journal Article, Review