Stanford study links macrophage failure to aging across organs
This digest was compiled by AI from multiple sources — links to the originals are below.
Stanford Medicine researchers found that tissue-resident macrophages lose the ability to clear senescent neutrophils with age, driving aging across organs. Blocking a single receptor on these macrophages kept multiple organs youthful in mice and reduced cognitive decline. The findings were published in Science.
Key Facts
- Tissue-resident macrophages become less able with age to dispose of senescent neutrophils, contributing to aging throughout the body.
- Blocking a single receptor on tissue-resident macrophages kept multiple organs youthful in mice, including the brain, heart, liver, and kidneys.
- Disabling the receptor in tissue-resident macrophages protected mice from frailty, excess fat accumulation, heart trouble, and cognitive decline.
- The receptor normally responds to a hormone involved in inflammation and pain in both mice and humans.
- The findings were published in Science, with Katrin Andreasson as senior author and Jessy Tan as lead author.
Macrophage Failure in Aging
Stanford Medicine researchers found that tissue-resident macrophages, immune cells that live permanently within organs, become less able with age to dispose of another class of immune cells called neutrophils. Neutrophils are the most abundant white blood cells and normally live only 12 to 24 hours before being cleared by macrophages in the liver, spleen, and bone marrow. In aging animals, most neutrophils that never encounter a pathogen quickly enter senescence, a dysfunctional state in which they release harmful chemicals that damage nearby cells and promote inflammation. Neutrophil numbers increase with age, and a growing proportion of them become senescent, placing a greater burden on macrophage clearance.
Receptor Blockade Effects
When the scientists blocked a single receptor on tissue-resident macrophages, multiple organs in mice retained more youthful characteristics, including the brain, heart, skeletal and heart muscle, liver, spleen, bone marrow, kidney, and colon. The receptor normally responds to a hormone involved in inflammation and pain in both mice and humans. Disabling the receptor specifically in tissue-resident macrophages protected mice from frailty, excess fat accumulation, and heart trouble. Cognitive decline was substantially reduced as well, according to Katrin Andreasson, MD, the Edward F. and Irene Thiel Pimley Professor in Neurology and Neurological Sciences.
Implications for Aging
The results provide new insight into the important role that chronic, body-wide inflammation plays in aging and its associated health problems. They also point toward a potential drug strategy that could slow age-related deterioration in organs and possibly extend the number of years people remain healthy. Katrin Andreasson stated, "We've been trying to figure out why we age. Now we know at least one big reason for it."
1 source
Time · lag behind first