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Inicio Revista Colombiana de Reumatología Smad y otros blancos terapéuticos en esclerodermia
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Vol. 18. Núm. 4.
Páginas 285-294 (Diciembre 2011)
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Vol. 18. Núm. 4.
Páginas 285-294 (Diciembre 2011)
DOI: 10.1016/S0121-8123(11)70044-5
Acceso a texto completo
Smad y otros blancos terapéuticos en esclerodermia
Smad and other therapeutic targets in scleroderma
Visitas
...
Adriana Lucía Vanegas1, Gloria María Vásquez2,
Autor para correspondencia
glomavas@gmail.com

Correspondencia.
1 internista, residente de Reumatología, Universidad de Antioquia, Medellín, Colombia
2 profesora sección de Reumatología, Universidad de Antioquia, Medellín, Colombia
Información del artículo
Resumen

La esclerodermia es una enfermedad caracterizada por la acumulación excesiva de tejido fibroso que lleva a alteración en la estructura y función de la piel y de órganos internos. La principal citoquina involucrada en este proceso es el factor transformante de crecimiento beta y sus funciones se realizan principalmente a través de la señalización intracelular mediada por las proteínas Smad. Se han desarrollado estrategias para bloquear los efectos del factor transformante de crecimiento beta y la identificación de la vía de transmisión de señales proporciona nuevas herramientas para la investigación de futuras terapias, pero son necesarios más estudios en modelos animales y en humanos que logren reproducir en forma satisfactoria y segura los resultados.

El propósito de este artículo es analizar la función del factor transformante de crecimiento beta en la fisiopatología de la esclerodermia profundizando en la vía de señalización mediada por Smad; además, revisar los estudios que involucran estas proteínas como blanco terapéutico de moléculas y medicamentos como posibles tratamientos para la esclerodermia.

Palabras clave:
esclerodermia sistémica
TGF-beta
proteínas Smad
imatinib
Key words:
systemic scleroderma
TGF-beta
Smad proteins
imatinib
Summary

Scleroderma is a disease characterized by excessive accumulation of fibrous tissue that leads to alteration in the structure and function of the skin and internal organs. The main cytokine involved in this process is the transforming growth factor beta and their functions are carried out mainly through intracellular signaling mediated by Smad proteins. Several strategies have been developed to block the effects of the transforming growth factor beta and understanding the signaling pathway provides new tools for the investigation of future therapies, but more studies are needed in animal models and humans to get the replication of the results in a satisfactory and safe manner.

The purpose of this paper is to analyze the role of the transforming growth factor beta in the pathophysiology of scleroderma emphasizing the signaling pathway mediated by Smad; it is also to review some studies involving these proteins as therapeutic targets of molecules and drugs that could become potential treatments for scleroderma.

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