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Todo lo que se sabe del envejecimiento en clave molecular
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Todo lo que se sabe del envejecimiento en clave molecular

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Todo lo que se sabe del envejecimiento en clave molecular

La revista Cell publica una revisión sobre estudios del envejecimiento, en la que se definen por primera vez todos los indicadores moleculares de este proceso en mamíferos. El estudio expone nueve firmas que marcan el avance del envejecimiento; y también, sobre cuáles se puede actuar para prolongar la vida. Los autores son María Blasco y Manuel Serrano, del Centro Nacional de Investigacones Oncológicas, Carlos López-Otín, de la Universidad de Oviedo, Linda Partridge, del Instituto Max Planck de Biología del Envejecimiento, y Guido Kroemer, de la Universidad de París Descartes.

Se han inspirado en el trabajo publicado también en Cell en 2000 que marcó un antes y un después en la investigación de esta enfermedad. "La situación en envejecimiento se parece mucho a la del cáncer en décadas pasadas", afirma el trabajo resultante: The Hallmarks of Aging. El paralalelismo con el cáncer va más lejos: uno de los principales resultados del artículo indica que entendiendo y combatiendo el envejecimiento se lucha también contra el cáncer. El envejecimiento resulta de la acumulación de daño en el ADN a lo largo de la vida, y ese proceso es también lo que origina el cáncer, la diabetes, las enfermedades cardiovasculares y las neurodegenerativas.

Los nueve marcadores moleculares del envejecimiento se clasifican en: primarios (causa desencadenante); los que conforman la respuesta del organismo a esas causas, y los fallos funcionales resultantes.

Causa, respuesta, fall

Las causas primarias del envejecimiento son la inestabilidad genómica, el acortamiento de los telómeros, las alteraciones epigenéticas y la pérdida de la proteostasis. Las respuestas del organismo a las causas desencadenantes son mecanismos que intentan corregir los daños, pero que, si se cronifican o exacerban, también se vuelven dañinos. Es el caso de la senescencia celular: induce a la célula a dejar de dividirse cuando acumula muchos defectos y así previene el cáncer, pero, en exceso, los tejidos envejecen. También tienen este doble filo otros dos procesos muy presentes en las discusiones sobre teorías del envejecimiento: el daño oxidativo, relacionado con los radicales libres, y mecanismos derivados del metabolismo, relacionados a su vez con las evidencias, no confirmadas en humanos, sobre al restricción calórica y la longevidad. Todo apunta a que la realidad es más compleja que simplemente dejar de comer para vivir más; en cuanto a los antioxidantes, los autores son tajantes: no hay evidencia genética de que elevar las defensas antioxidantes retrase el envejecimiento.

El tercer grupo de indicadores aparece  cuando los daños causados por los dos precedentes no pueden ser compensados. Es el caso del agotamiento de las células madre de los tejidos o de los errores en la comunicación intercelular.

A partir de este conocimiento habrá que diseñar estrategias terapéuticas; una ya probada en ratones, con éxito, es evitar el acortamiento de los telómeros. "Es un proceso que se puede frenar e incluso revertir en ratones", afirma Blasco. Ella cree que, en general, "tenemos aún mucho margen de maniobra para combatir el envejecimiento y lograr vivir más años de forma saludable".

Un gen para la pluripotencia y otro para el cáncer

Esta semana el CNIO participa en otros dos estudios que aparecen en revistas destacadas. El grupo de María Blasco ha descubierto, según refieren en Nature Communications, un nuevo gen esencial para la reprogramación celular: el TRF1 es indispensable para proteger a los telómeros, cuya longitud ya se había relacionado con la pluripotencia. Y en Molecular Biology and Evolution, el grupo de Alfonso Valencia, también en el CNIO, ha hallado cómo una duplicación genética, hace millones de años, permitió la evolución del gen ASF1b, implicado en el cáncer.

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