Immune-specific aging drives senescence and dysfunction of peripheral tissues
Aging is generally thought to be driven by an accumulation of damage in cells over time. This damage triggers stress responses in cells culminating in cell death or senescence. Senescence is potently triggered in response to DNA damage, and prevents a cell from copying their damaged genome, which reduces the risk of cancer. But these senescent cells secrete factors that drive inflammation and aging. Dr. Yousefzadeh discovered that if you allow DNA damage that naturally occurs in the immune cells of mice to go unrepaired, this is enough to cause them to undergo senescence. The senescent immune cells then drive tissue dysfunction in many organs (kidney, liver, muscle, etc.). In the proposed project, he plans to define this novel mechanism of cell non-autonomous aging so that we can create new therapeutic aging targets.
