2003, Número 2
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Gac Med Mex 2003; 139 (2)
Receptores y funciones del TGF-beta, una citocina crucial en la cicatrización.
García-Sainz JA, Vilchis-Landeros MM, Juárez P, López-Casillas F, Hernández-Pando R, López-Casillas F, Massagué J
Idioma: Español
Referencias bibliográficas: 134
Paginas: 126-143
Archivo PDF: 176.31 Kb.
FRAGMENTO
Introducción
Una de las complicaciones más frecuentes y generalmente fatal
de la diabetes mellitus es la insuficiencia renal. Éste es un grave problema de
salud en México, pues no sólo su incidencia va en aumento, sino que la población
mexicana parece ser particularmente susceptible a ella. Garza y colaboradores
han encontrado que en los pacientes diabéticos tipo II (no dependientes de insulina)
de origen mexicano, el deterioro de la función renal es más acelerado que en grupos
de diferente origen étnico. En la década pasada el entendimiento de la fisiopatología
de la nefropatía, de etiología diabética en particular y de otras etiologías en
general, ha revelado que uno de los principales mediadores del daño renal es una
poderosa citocina llamada Transforming Growth Factor tipo beta (TGF-β).
3,4
De ahí que, en principio, un tratamiento racional de las nefropatías debería basarse
en inhibidores del TGF-β, los cuales, necesariamente, resultarán del conocimiento
derivado de los mecanismos de señalamiento del TGF-β. Este campo de estudio
ha tenido un desarrollo espectacular en los últimos años con el consecuente desarrollo
de nuevos conceptos y la identificación de moléculas transductoras de sus señales,
las cuales podrían ser blancos para una intervención terapéutica anti-TGF-β.
En esta parte del simposio discutiremos conceptos básicos de la biología del TGF-β,
sus mecanismos fisiopatológicos, y los agentes neutralizadores del TGF-β
más promisorios para una eventual terapia en humanos.
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II. Participación del factor de transformación tumoral- en la regulación de la inflamación y la respuesta inmunológica
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