Abstract
Oxygen metabolism is thought to impact on aging through the formation of reactive oxygen species (ROS) that are supposed to damage biological molecules. The study of p66(Shc), a crucial regulator of ROS level involved in aging dysfunction, suggests that the incidence of degenerative disease and longevity are determined by a specific signaling function of ROS other than their unspecific damaging property.
Highlights
The reason why we age seems obvious: entropy increases
Oxygen metabolism is thought to impact on aging through the formation of reactive oxygen species (ROS) that are supposed to damage biological molecules
Our contribution to this field arises from the study of p66Shc, the first protein identified whose deletion in mouse prolongs life span and protects from a variety of agingassociated diseases without showing apparent negative effects
Summary
The reason why we age seems obvious: entropy increases. The reason why different species are differently affected by passing of equal time should be apparent as well: genetic and epigenetic variability. The study of p66Shc, a crucial regulator of ROS level involved in aging dysfunction, suggests that the incidence of degenerative disease and longevity are determined by a specific signaling function of ROS other than their unspecific damaging property.
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