Longevity & AgingLiver Protein MLKL Drives Aging Through Mitochondrial Damage and Cellular Senescence
Researchers discovered that MLKL, a protein previously known for its role in inflammatory cell death, has a surprising second job in liver aging. When elevated in liver cells, MLKL doesn't kill them — instead it impairs mitochondria, generates oxidative stress, and triggers cellular senescence, a state where cells stop dividing but pump out inflammatory signals. These senescent cells then release extracellular vesicles that spread the senescent state to neighboring cells, including immune macrophages, amplifying liver inflammation. The findings identify MLKL as a key driver of age-related liver disease and a potential drug target for conditions like fatty liver disease associated with aging.
