musculoPara mantener la fuerza muscular las células deben deshacerse de los desperdicios que se acumulan en ellas con el tiempo. Así lo indica un nuevo estudio realizado por investigadores de la Universidad de Pádova (Italia) y publicado en el último número de la revista Cell Metabolism, que muestran cómo en el caso de las células este material de desecho se compone de restos de orgánulos, grupos tóxicos de proteínas y patógenos.
«Si hay un fallo del sistema encargado de eliminar lo que está dañado, y éste persiste, la fibra muscular no está a gusto», explica Marco Sandri, autor principal del estudio e investigador de la Universidad de Padua en Italia. Las proteínas dañadas y mal plegadas se acumulan junto con mitocondrias disfuncionales, retículo endoplásmico distendido, radicales libres y otras estructuras anómalas. Finalmente, algunas de las células musculares mueren y «los músculos se vuelven cada vez más débiles con la edad».

Los investigadores analizaron ratones con deficiencia de un gen requerido para el proceso estrictamente controlado de degradación y reciclaje dentro de las células, conocido como autofagia. Los animales mostraron atrofia muscular profunda y debilidad muscular que empeoraba con la edad.

Según Sandri, la pérdida de masa muscular observada en los ratones parece tener cierta semejanza con ciertas formas de enfermedades de degeneración muscular. «Este tipo de mecanismo puede ofrecer conocimientos sobre algunas de las enfermedades todavía inexplicables, así como del debilitamiento muscular que sobreviene con el envejecimiento normal (una condición conocida como sarcopenia)», sostiene.

Los expertos ya conocían que la autofagia excesiva también puede conducir a la pérdida de masa muscular y a la enfermedad. Ahora, los nuevos resultados destacan la importancia del mantenimiento de un nivel normal de autofagia para eliminar los desechos y mantener una correcta función muscular.

Aunque el descubrimiento parece tener toda su lógica visto ahora, no era lo que el equipo de Sandri había previsto inicialmente. «Pensábamos que reducir la autofagia podía proteger contra la atrofia», señaló. «En cambio, es todo lo contrario. Nos dimos cuenta, por supuesto, de que si no se elimina el daño, provoca la debilidad».

Los hallazgos podrían tener repercusiones clínicas en el desarrollo de terapias para bloquear la degradación de las proteínas en ciertos trastornos de degeneración muscular. Aunque en algunos casos, al menos, «puede ser mejor activar la autofagia y eliminar la basura en las células», concluye Sandri.

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