Bullon, PedroAlcocer-Gomez, ElisabetCarrion, Angel MMarin-Aguilar, FabiolaGarrido-Maraver, JuanRoman-Malo, LourdesRuiz-Cabello, JesusCulic, OgnjenRyffel, BernhardApetoh, LionelGhiringhelli, FrançoisBattino, MaurizioSanchez-Alcazar, Jose AntonioCordero, Mario D2023-01-252023-01-252016-01-19Bullón 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.http://hdl.handle.net/10668/9927Impairment 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.enAMP-Activated Protein KinasesCarrier ProteinsFibromyalgiaInterleukin-18MicePain PerceptionSunitinibAdultAnimalsFemaleHumansIndolesInflammasomesInterleukin-1betaMaleMetforminMiddle AgedNLR Family, Pyrin Domain-Containing 3 ProteinPainPhosphorylationPyrrolesresearch article26132721Restricted AccessInflamasomasDolor crónicoHiperalgesiaProteínas QuinasasDominio PirinaTerapéuticaSunitinibAdenosina monofosfatoProteínas NLR10.1089/ars.2014.61201557-7716PMC4742979https://europepmc.org/articles/pmc4742979?pdf=renderhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC4742979/pdf