Clara Correia-Melo, Graeme Hewitt and João F Passos
Abstract (provisional)
Senescence, the state of irreversible cell-cycle arrest, plays paradoxical albeit important roles in vivo: it protects organisms against cancer but also contributes to age-related loss of tissue function. The DNA damage response (DDR) has a central role in cellular senescence. Not only does it contribute to the irreversible loss of replicative capacity but also to the production and secretion of reactive oxygen species (ROS), and bioactive peptides collectively known as the senescence-associated secretory phenotype (SASP). Both ROS and the SASP have been shown to impact on senescence in an autocrine as well as paracrine fashion; however, the underlying mechanisms are not well understood. In this review we describe our current understanding of cellular senescence, examine in detail the intricate pathways linking the DDR, ROS and SASP, and evaluate their impact on the stability of the senescent phenotype.
The complete article is available as a provisional PDF. The fully formatted PDF and HTML versions are in production.
This makes perfect sense in the light that ecsexire has never seemed to increase maximum lifespan in animal models.However, we know that ecsexire increases healthspan so no reason to cut it out yet.This also starts to make me think about people who take hormone replacement therapy. My gut feeling is that an increase in growth hormones increases muscle mass which in term might increase ROS damage to DNA. Once again increasing healthspan vs lifespan. The real kicker would be to do a study on hormone replacement vs ecsexire in older animals — who would live longer (and at what healthspan).