Inhibition of ATM Kinase Reduces Cellular Senescence and SASP in Progeroid Mice

Progeroid mice with DNA repair deficiencies exhibit an accelerated formation of senescent cells and manifestation of age-related conditions. This class of animal model has been used in research relating to cellular senescence in order to cost-effectively demonstrate that targeted removal of senescent cells is beneficial. However, one still needs to be careful when drawing conclusions based on their peculiar biochemistry. Progeria of this nature is quite unlike normal aging at the detail level. Cells become senescent in response to reaching the Hayflick limit, tissue injury, molecular damage, or a toxic environment. A senescent cell ceases replication and generates senescence-associated secretory phenotype (SASP), a mix of signals that encourages both tissue remodeling and an immune response to destroy the senescent cell. In young people near all senescent cells are efficiently destroyed soon after their creation, but in older people senescent cells linger to cause chronic inflammation and tissue dysfunction. A great deal of effort is going into deeper explorations of the biochemistry of cellular senescence these days. This is in no small part because any new discovery might have the potential to become a therapy that can treat numerous age-related conditions, and even aging itself, by alleviating the burden of senescent cells and their inflammatory, harmful signaling. Researchers here identify an important regulator gene linking DNA damage with cellular s...
Source: Fight Aging! - Category: Research Authors: Tags: Medicine, Biotech, Research Source Type: blogs