Investigadores de Israel logran avances en la lucha para curar el lupus.

El lupus es una enfermedad autoinmune crónica que puede atacar varias partes del cuerpo. Según la Fundación Lupus, hay cinco millones de casos en todo el mundo. Esta avance puede ayudar también para la cura del Alzheimer.

La profesora Varda Shoshan-Barmatz, en colaboración con un grupo de NIH, encabezado por el Dr. Jay Chung, ha tenido un éxito notable en modelos de ratones con lupus. Ahora están comenzando a dar los siguientes pasos hacia otras enfermedades.

Los investigadores han logrado demostrar que la proteína mitocondrial VDAC1 es crítica para la liberación del ADN mitocondrial (ADNmt) asociado con la patología de la enfermedad de Lupus.

Además, demostraron que la inhibición de VDAC1 por una molécula pequeña recientemente desarrollada, resultó en una mejora sustancial en los aspectos patológicos de la enfermedad.

En su trabajo han identificado el camino que utiliza el ADN mitocondrial para salir de las células para desencadenar enfermedades autoinmunes y cómo bloquear esa ruta de escape.

Los investigadores han demostrado su concepto en Lupus y sus hallazgos se informaron en Science el 20 de diciembre.

El descubrimiento es un mecanismo único que involucra el canal aniónico dependiente del voltaje de la proteína mitocondrial (VDAC1) en la salida de factores mitocondriales como las proteínas de muerte procelular y el ADN mitocondrial (ADNmt) que desencadenan algunas enfermedades autoinmunes.

Cuando VDAC1 se sobreexpresa, como se encuentra en varias enfermedades, se forma un poro grande compuesto por varias unidades VDAC1, lo que permite la liberación de factores de muerte procelulares y ADNmt.

La profesora Shoshan-Barmatz ha desarrollado una molécula llamada VBIT-4 que inhibe la muerte celular y restaura las funciones mitocondriales asociadas con varias enfermedades.

Esa nueva molécula evita la formación del gran poro causado por la sobreexpresión de VDAC1 y, por lo tanto, evita la salida de estos factores de las mitocondrias.

Sin la liberación de estos factores, se evita la muerte celular en enfermedades como las enfermedades de Alzheimer y Parkinson, o la liberación de ADNmt como en el lupus.

“Nuestro avance es identificar una nueva vía para la salida del ADN mitocondrial que podemos activar en condiciones controladas o inhibir utilizando nuestra nueva molécula que desarrollamos específicamente para prevenir la formación de esta vía”, dice la profesora Shoshan.

“Dado que los resultados hasta ahora con el lupus han sido tan prometedores, creemos que la molécula será beneficiosa para otras enfermedades como el Alzheimer, la enfermedad de Crohn y la colitis ulcerosa. Estas suposiciones vienen respaldadas por nuestos resultados preliminares”, agrega.

También se ha encontrado ADNmt en el plasma de pacientes de otras enfermedades autoinmunes como la colitis y las enfermedades de Crohn.

Esto genera nuevas esperanzas de que esta molécula moduladora de VDAC1 conduzca a más terapias en una lista en expansión de otras enfermedades que están asociadas con la muerte celular o la liberación de ADN de las mitocondrias.

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