2026-07-21T14:27:02Zhttps://repisalud.isciii.es/rest/oai/requestoai:repisalud.isciii.es:20.500.12105/72592024-09-27T10:11:58Zcom_20.500.12105_19604com_20.500.12105_2051col_20.500.12105_19607
Repisalud
author
Pavillard, Luís E
author
Cañadas-Lozano, Diego
author
Alcocer-Gómez, Elísabet
author
Marín-Aguilar, Fabiola
author
Pereira, Sheila
author
Robertson, Avril A B
author
Muntané, Jordi
author
Ryffel, Bernhard
author
Cooper, Matthew A
author
Quiles, José L
author
Bullón, Pedro
author
Ruiz-Cabello, Jesus
author
Cordero, Mario D
funder
Regional Government of Andalusia (España)
2019-02-28T15:37:44Z
2019-02-28T15:37:44Z
2017-11-21
Oncotarget. 2017; 8(59):99740-99756
10.18632/oncotarget.20763
1949-2553
1949-2553
Oncotarget
29245937
http://hdl.handle.net/20.500.12105/7259
The NLRP3-inflammasome complex has emerged as an important component of inflammatory processes in metabolic dysfunction induced by high-caloric diets. In this study, we investigate the molecular mechanisms by which NLRP3 inhibition may attenuate diet-induced cardiac injury. Here we show the cardiac damage induced by high sugar diet (HSD), high fat diet (HFD) or high sugar/fat diet (HSFD) over 15 weeks. Genetic ablation of NLRP3 protected against this damage by autophagy induction and apoptotic control. Furthermore, NLRP3 inhibition by the selective small molecule MCC950 resulted in similar autophagy induction and apoptotic control in hearts after diets. These data were reproduced in THP-1 cells treated with MCC950 and cultured in media supplemented with serum from mice dosed with MCC950 and fed with diets. NLRP3 inhibition exerted beneficial metabolic, and autophagic adaptations in hearts from obesogenic diets. The inhibition of NLRP3 activation may hold promise in the treatment of metabolic and cardiovascular diseases.
eng
MCC950
NLRP3-inflammasome
Autophagy
Cardiac damage
NLRP3-inflammasome inhibition prevents high fat and high sugar diets-induced heart damage through autophagy induction
journal article
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