2014, Número 2
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Neumol Cir Torax 2014; 73 (2)
Participación de las metaloproteinasas de matriz extracelular en la EPOC
Hernández-Montoya J, Pérez-Rubio G, Pérez RJ, Montaño RM, Ramos AC, Ramírez VA, Camarena Á, Sansores R, Falfán-Valencia R
Idioma: Español
Referencias bibliográficas: 95
Paginas: 128-137
Archivo PDF: 305.20 Kb.
RESUMEN
En la enfermedad pulmonar obstructiva crónica (EPOC) se presentan dos fenotipos clínicos, enfisema y bronquitis crónica. Tales fenotipos comparten síntomas clínicos como la disnea y la obstrucción bronquial al flujo de aire, además de un aumento de células de la inmunidad innata (macrófagos y neutrófilos), liberación de múltiples mediadores de la inflamación (quimiocinas, citocinas, factores de crecimiento), estrés oxidativo, aumento de metaloproteinasas de matriz extracelular (MMPs) en las vías aéreas y el pulmón. La progresión de la enfermedad se asocia con la presencia de inflamación crónica y aumento de la actividad proteolítica de enzimas como las MMPs que resulta en la degradación de las fibras de elastina y colágeno en las paredes de los alvéolos y la matriz extracelular del pulmón.
De especial interés para esta revisión ha sido describir la función de las MMPs, su participación en el desarrollo de la EPOC, tanto en la destrucción de la matriz extracelular y la remodelación anormal del pulmón dañado. También se mencionan estudios de asociación genética de polimorfismos tipo SNP (polimorfismo de un solo nucleótido) en MMPs, en poblaciones como la caucásica con el desarrollo y la progresión de la EPOC, además de la importancia de llevar a cabo estudios en poblaciones mestizas. La función de las MMPs también se ha conocido a través de modelos animales como ratones knock-out para MMPs expuestos a humo de cigarro. Todos estos estudios implican a las MMPs como mediadores clave en la patogénesis de la EPOC. Finalmente, el estudio de las MMPs permitirá la base para futuras terapias, posibles blancos terapéuticos y tratamientos de la enfermedad.
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