TY  - JOUR
A1  - Anderson, Rozalyn
A1  - Cordero, Mario D.
A1  - Bullón, Pedro
A1  - Ruiz-Cabello, Jesús
A1  - Robertson, Avril A B
A1  - Ryffel, Bernhard
A1  - Pérez-Pulido, Antonio J
A1  - Muntané, Jordi
A1  - Pérez-Alegre, Mónica
A1  - Andújar-Pulido, Eloísa
A1  - de la Cruz, Patricia
A1  - Cooper, Matthew A
A1  - Lendines-Cordero, Debora
A1  - Alcocer-Gómez, Elísabet
A1  - Castejón-Vega, Beatriz
A1  - Marín-Aguilar, Fabiola
JF  - The Journals of Gerontology: Series A
EP  - 1464
ID  - uneatlantico122
AV  - none
IS  - 8
SP  - 1457
Y1  - 2019///
KW  - NLRP3 inflammasome; Aging; Autophagy; MCC950; PPAR?.
UR  - http://doi.org/10.1093/gerona/glz239
N2  - 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-? 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-?. 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.
TI  - NLRP3 Inflammasome Inhibition by MCC950 in Aged Mice Improves Health via Enhanced Autophagy and PPAR? Activity
VL  - 75
SN  - 1079-5006
ER  -