@article{uneatlantico122,
          number = {8},
           title = {NLRP3 Inflammasome Inhibition by MCC950 in Aged Mice Improves Health via Enhanced Autophagy and PPAR{\ensuremath{\alpha}} Activity},
           pages = {1457--1464},
          author = {Rozalyn Anderson and Mario D. Cordero and Pedro Bull{\'o}n and Jes{\'u}s Ruiz-Cabello and Avril A B Robertson and Bernhard Ryffel and Antonio J P{\'e}rez-Pulido and Jordi Muntan{\'e} and M{\'o}nica P{\'e}rez-Alegre and Elo{\'i}sa And{\'u}jar-Pulido and Patricia de la Cruz and Matthew A Cooper and Debora Lendines-Cordero and El{\'i}sabet Alcocer-G{\'o}mez and Beatriz Castej{\'o}n-Vega and Fabiola Mar{\'i}n-Aguilar},
          volume = {75},
         journal = {The Journals of Gerontology: Series A},
            year = {2019},
        keywords = {NLRP3 inflammasome; Aging; Autophagy; MCC950; PPAR{\ensuremath{\alpha}}.},
        abstract = {The NLRP3 inflammasome has emerged as an important regulator of metabolic disorders and age-related diseases in NLRP3-deficient mice. In this article, we determine whether, in old mice C57BL6J, the NLRP3 inflammasome inhibitor MCC950 is able to attenuate age-related metabolic syndrome to providing health benefits. We report that MCC950 attenuates metabolic and hepatic dysfunction in aged mice. In addition, MCC950 inhibited the Pi3K/AKT/mTOR pathway, enhanced autophagy, and activated peroxisome proliferator-activated receptor-{\ensuremath{\alpha}} in vivo and in vitro. The data suggest that MCC950 mediates the protective effects by the mammalian target of rapamycin inhibition, thus activating autophagy and peroxisome proliferator-activated receptor-{\ensuremath{\alpha}}. In conclusion, pharmacological inhibition of NLRP3 in aged mice has a significant impact on health. Thus, NLRP3 may be a therapeutic target of human age-related metabolic syndrome.},
             url = {http://repositorio.uneatlantico.es/id/eprint/122/}
}