Autor según el artículo: Joven, J. Alonso-Villaverde, C. Camps, J. Garcia-Heredia, A. Aragones, G. Sierra-Filardi, E. Corbi, A. Martin Paredero, V. Sirvent, J. Vazquez-Martin, A. Menendez, J. Luciano, F. Beltran, R. Rull, A. Mariné, R. Hernandez-Aguilera, A. Riera, M. Rodriguez-Gallego, E.

Departamento: Bioquímica i Biotecnologia Medicina i Cirurgia Ciències Mèdiques Bàsiques

e-ISSN: 1466-1861

Autor/es de la URV: Esther Rodríguez-Gallego, Marta Riera-Borrull, Anna Hernández-Aguilera,Roger Mariné-Casadó, Anna Rull, Raúl Beltrán-Debón,Fedra Luciano-Mateo, Javier A. Menendez, Alejandro Vazquez-Martin, Juan J. Sirvent,Vicente Martín-Paredero, Angel L. Corbí, Elena Sierra-Filardi, Gerard Aragonès, Anabel García-Heredia, Jordi Camps, Carlos Alonso-Villaverde, Jorge Joven

Resumen: Excessive energy management leads to low-grade, chronic inflammation, which is a significant factor predicting noncommunicable diseases. In turn, inflammation, oxidation, and metabolism are associated with the course of these diseases; mitochondrial dysfunction seems to be at the crossroads of mutual relationships. The migration of immune cells during inflammation is governed by the interaction between chemokines and chemokine receptors. Chemokines, especially C-C-chemokine ligand 2 (CCL2), have a variety of additional functions that are involved in the maintenance of normal metabolism. It is our hypothesis that a ubiquitous and continuous secretion of CCL2 may represent an animal model of low-grade chronic inflammation that, in the presence of an energy surplus, could help to ascertain the afore-mentioned relationships and/or to search for specific therapeutic approaches. Here, we present preliminary data on a mouse model created by using targeted gene knock-in technology to integrate an additional copy of the CCl2 gene in the Gt(ROSA)26Sor locus of the mouse genome via homologous recombination in embryonic stem cells. Short-term dietary manipulations were assessed and the findings include metabolic disturbances, premature death, and the manipulation of macrophage plasticity and autophagy. These results raise a number of mechanistic questions for future study.

Acceso a la licencia de uso: https://creativecommons.org/licenses/by/3.0/es/

ISSN: 0962-9351

Página final: 18

Volumen de revista: 2013

Versión del articulo depositado: info:eu-repo/semantics/publishedVersion

Enlace a la fuente original: http://www.hindawi.com/journals/mi/2013/953841/

DOI del artículo: http://dx.doi.org/10.1155/2013/953841

Entidad: Universitat Rovira i Virgili.

Año de publicación de la revista: 2013

Página inicial: 1