GDF11 administration does not extend lifespan in a mouse model of premature aging

Abstract

// Sandra Freitas-Rodríguez 1 , Francisco Rodríguez 1 and Alicia R. Folgueras 1 1 Departamento de Bioquímica y Biología Molecular, Facultad de Medicina, Instituto Universitario de Oncología del Principado de Asturias (IUOPA), Universidad de Oviedo, Oviedo, Spain Correspondence to: Alicia R. Folgueras, email: // Keywords : progeria, accelerated aging, GDF11, longevity, Gerotarget Received : May 25, 2016 Accepted : July 22, 2016 Published : August 05, 2016 Abstract GDF11 has recently emerged as a powerful anti-aging candidate, found in young blood, capable of rejuvenating a number of aged tissues, such as heart, skeletal muscle and brain. However, recent reports have shown contradictory data questioning its capacity to reverse age-related tissue dysfunction. The availability of a mouse model of accelerated aging, which shares most of the features occurring in physiological aging, gives us an excellent opportunity to test in vivo therapies aimed at extending lifespan both in pathological and normal aging. On this basis, we wondered whether the proposed anti-aging functions of GDF11 would have an overall effect on longevity. We first confirmed the existence of a reduction in GDF11/8 levels in our mouse model of accelerated aging compared with wild-type littermates. However, we show herein that GDF11 daily administration does not extend lifespan of premature-aged mice.