Publication:
AMPK Phosphorylation Modulates Pain by Activation of NLRP3 Inflammasome.

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Date

2016-01-19

Authors

Bullon, Pedro
Alcocer-Gomez, Elisabet
Carrion, Angel M
Marin-Aguilar, Fabiola
Garrido-Maraver, Juan
Roman-Malo, Lourdes
Ruiz-Cabello, Jesus
Culic, Ognjen
Ryffel, Bernhard
Apetoh, Lionel

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Mary Ann Liebert, Inc. Publishers
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Abstract

Impairment in adenosine monophosphate-activated protein kinase (AMPK) activity and NOD-like receptor family, pyrin domain containing 3 (NLRP3) inflammasome activation are associated with several metabolic and inflammatory diseases. In this study, we investigated the role of AMPK/NLRP3 inflammasome axis in the molecular mechanism underlying pain perception. Impairment in AMPK activation induced by compound C or sunitinib, two AMPK inhibitors, provoked hyperalgesia in mice (p These data suggest that AMPK/NLRP3 inflammasome axis participates in chronic pain and that NLRP3 inflammasome inhibition by AMPK modulation may be a novel therapeutic target to fight against chronic pain and inflammatory diseases as FM.

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MeSH Terms

Adult
Animals
Female
Humans
Indoles
Inflammasomes
Interleukin-1beta
Male
Metformin
Middle Aged
NLR Family, Pyrin Domain-Containing 3 Protein
Pain
Phosphorylation
Pyrroles

DeCS Terms

Inflamasomas
Dolor crónico
Hiperalgesia
Proteínas Quinasas
Dominio Pirina
Terapéutica
Sunitinib
Adenosina monofosfato
Proteínas NLR

CIE Terms

Keywords

AMP-Activated Protein Kinases, Carrier Proteins, Fibromyalgia, Interleukin-18, Mice, Pain Perception, Sunitinib

Citation

Bullón P, Alcocer-Gómez E, Carrión AM, Marín-Aguilar F, Garrido-Maraver J, Román-Malo L, et al. AMPK Phosphorylation Modulates Pain by Activation of NLRP3 Inflammasome. Antioxid Redox Signal. 2016 Jan 20;24(3):157-70.