Why do we age? As we have discussed before, natural selection tends to favor molecular processes that enhance health and reproductive fitness in youth. However, these genetic programs can also come with unselected negative effects on physical function later in life.
A good example of this is cellular senescence. When exposed to certain forms of stress (like DNA damage), normal cells enter a senescent state, in which they no longer divide. This, generally speaking, is a good thing – cellular senescence probably evolved as a protective mechanism against cancer.
However, senescent cells tend to accumulate as people get older, and they cause all kinds of trouble. They release inflammatory molecules and other factors that speed up the aging process. Not so great.
In this episode of humanOS Radio, I interview Judith Campisi. Dr. Campisi is a professor of biogerontology at the Buck Institute for Research on Aging.
Recently, she and a team of researchers found that selectively removing senescent cells from the joints of injured rodents enhanced cartilage repair in the damaged site and prevented the development of osteoarthritis. What other age-related conditions might be responsive to this therapeutic approach? Listen below to find out more!