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>Revistas >Gaceta Médica de México >Año 2007, No. 6


Bastarrachea RA, López-Alvarenga JC, Bolado-García VE, Téllez-Mendoza J, Laviada-Molina H, Comuzzie AG
Macrófagos, inflamación, tejido adiposo, obesidad y resistencia a la insulina
Gac Med Mex 2007; 143 (6)

Idioma: Español
Referencias bibliográficas: 54
Paginas: 505-512
Archivo PDF: 80.69 Kb.


Texto completo




RESUMEN

La obesidad se asocia con un estado inflamatorio implicado en el desarrollo de aterosclerosis y resistencia a la insulina. Los macrófagos son claves en la génesis de estos procesos. La obesidad induce la acumulación de macrófagos en el tejido adiposo. Los macrófagos producen muchas de las moléculas inflamatorias secretadas por el tejido adiposo. Las proteínas quimioatrayentes de monocitos (MCP) y sus receptores son fundamentales en la respuesta inflamatoria y en el reclutamiento de células inmunes en sitios de inflamación. La expresión en el tejido adiposo de una MCP, la quimiocina del ligando 2 del motif C-C (CCL2 o MCP1), está incrementada en proporción a la adiposidad. El receptor 2 de quimiocina del motif C-C (CCR2) regula el reclutamiento y quimiotaxis de monocitos y macrófagos, es necesario para las respuestas inflamatorias dependientes de macrófagos y para el desarrollo de aterosclerosis. Ya que el receptor CCR2 regula las respuestas inflamatorias locales, se ha postulado que las MCP, actuando a través de su receptor CCR2, podrían regular la inflamación inducida por la obesidad en el tejido adiposo. Este documento se enfoca en dilucidar los mecanismos moleculares y genéticos que permiten reclutar y retener macrófagos en el tejido adiposo.


Palabras clave: Adipocito, macrófago, inflamación, disfunción endotelial, resistencia a la insulina, MCP1.


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>Revistas >Gaceta Médica de México >Año2007, No. 6
 

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