Literature DB >> 26462871

The voltage-gated sodium channel NaV 1.9 in visceral pain.

J R F Hockley1,2, W J Winchester3, D C Bulmer1,2.   

Abstract

BACKGROUND: Visceral pain is a common symptom for patients with gastrointestinal (GI) disease. It is unpleasant, debilitating, and represents a large unmet medical need for effective clinical treatments. Recent studies have identified NaV 1.9 as an important regulator of afferent sensitivity in visceral pain pathways to mechanical and inflammatory stimuli, suggesting that NaV 1.9 could represent an important therapeutic target for the treatment of visceral pain. This potential has been highlighted by the identification of patients who have an insensitivity to pain or painful neuropathies associated with mutations in SCN11A, the gene encoding voltage-gated sodium channel subtype 1.9 (NaV 1.9).
PURPOSE: Here, we address the role of NaV 1.9 in visceral pain and what known human NaV 1.9 mutants can tell us about NaV 1.9 function in gut physiology and pathophysiology.
© 2015 John Wiley & Sons Ltd.

Entities:  

Keywords:  NaV1.9; enteric nervous system; inflammatory bowel disease; irritable bowel syndrome; nociceptor sensitivity; visceral afferent; visceral pain; voltage-gated sodium channel

Mesh:

Substances:

Year:  2015        PMID: 26462871     DOI: 10.1111/nmo.12698

Source DB:  PubMed          Journal:  Neurogastroenterol Motil        ISSN: 1350-1925            Impact factor:   3.598


  11 in total

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10.  Protein arginine methyltransferase 7 modulates neuronal excitability by interacting with NaV1.9.

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Journal:  Pain       Date:  2022-04-01       Impact factor: 7.926

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