Research team at Osaka University in Japan find gene reversal at cellular level possible. As we grow old cells transition to senescence cells.

UCLA scientists have discovered a population of senescent “zombie” immune cells, specifically macrophages marked by p21 and TREM2 proteins, that accumulate in aging livers and drive chronic inflammation and fatty liver disease. In older mice, these dysfunctional cells can make up 60-80% of liver macrophages, compared to just 5% in young mice. The study found that excess cholesterol from high-fat diets accelerates this senescence process, turning normally protective macrophages into inflammatory drivers that worsen metabolic dysfunction-associated steatotic liver disease. When researchers used the senolytic drug ABT-263 to selectively eliminate these senescent macrophages, the results were striking: liver size normalized, inflammation dropped sharply, and fatty liver damage reversed dramatically even while the mice continued eating an unhealthy diet. Body weight also decreased by about 25%. Analysis of human liver biopsy data showed the same senescent macrophage signature is elevated in people with fatty liver disease. The findings support the geroscience idea that targeting core aging processes like cellular senescence could treat multiple age-related conditions, including fatty liver disease, atherosclerosis, and Alzheimer’s. While ABT-263 is too toxic for human use, the team is now searching for safer compounds. This research highlights macrophage senescence as a promising therapeutic target for both aging and metabolic liver disease, which affects 30-40% of people in areas like Los Angeles.

Senescent “zombie” cells are linked to aging and multiple diseases, but spotting them in living tissue has been notoriously difficult. Researchers at Mayo Clinic have now taken an inventive leap by us...

ファンケルは独自の研究から、龍牙草・仙鶴草とも呼ばれ、伝統的に中国医学でも使用されるバラ科の食品素材「キンミズヒキ」およびキンミズヒキ由来のポリフェノール、アグリモール類に老化した細胞を除去する作用を見いだしている。老化...