A prostaglandin prevents macrophages from clearing toxic neutrophils in aging organs
Abstract
Human aging is asynchronous. Cells, tissues, and organs deteriorate at different rates, an unevenness that may help explain the differential aging trajectories of people. Elucidating both the overlapping and distinct biological pathways that contribute to cell-tissue-organ aging could guide strategies to promote health longevity. On page 264 of this issue, Tan et al. (1) report that the oxylipin prostaglandin E2 (PGE2) undermines the capacity of tissue-resident macrophages (TRMs) from clearing out old, and hence damaging, neutrophils in aging organs. In a mouse model, this housekeeping process can be restored if PGE2 action is blocked. The implication is that organ aging is not fixed but may be shaped by specific interventions that slow the decline. Its paywalled at:
https://www.science.org/doi/10.1126/science.aei9816
