TAp73 depletion accelerates aging through metabolic dysregulation

Aging is associated with impaired scavenging of reactive oxygen species (ROS). Here, we show that TAp73, a p53 family member, protects against aging by regulating mitochondrial activity and preventing ROS accumulation. TAp73-null mice show more pronounced aging with increased oxidative damage and senescence. TAp73 deletion reduces cellular ATP levels, oxygen consumption, and mitochondrial complex IV activity, with increased ROS production and oxidative stress sensitivity. We show that the mitochondrial complex IV subunit cytochrome C oxidase subunit 4 (Cox4i1) is a direct TAp73 target and that Cox4i1 knockdown phenocopies the cellular senescence of TAp73-null cells. Results indicate that TAp73 affects mitochondrial respiration and ROS homeostasis, thus regulating aging.     

What (or who) causes health inequalities: Theories,evidence and implications?

Health inequalities are the unjust differences in health between groups of people occupying different positions in society. Since the Black Report of 1980 there has been considerable effort to understand what causes them, so as to be able to identify actions to reduce them. This paper revisits and updates the proposed theories, evaluates the evidence in light of subsequent epidemiological research, and underlines the political and policy ramifications.