Non-death MLKL drives stem cell aging by damaging mitochondria
Researchers at the University of Tokyo and St. Jude found that aging-related stress activates MLKL in hematopoietic stem cells not to kill them, but to damage mitochondria, weakening self-renewal and skewing blood cell production toward myeloid cells. Inactivating MLKL preserved stem cell function under stress, suggesting mitochondrial-protective or necroptosis‑modulating therapies could help maintain blood/immune health during aging or after chemotherapy/transplantation.
