All articles tagged with #senescent macrophages
UCLA researchers report that in mice, removing a senescent macrophage population—zombie cells—reverses fatty liver disease even on an unhealthy diet, a finding that could reshape treatment for millions of LA residents, though human trials are still needed.
UCLA researchers identify a population of p21+ TREM2+ senescent macrophages that drive liver inflammation and fatty liver; removing them in mice on a fatty/high-cholesterol diet reverses liver damage and inflammation without changing diet, using the senolytic drug ABT-263. However, ABT-263 is too toxic for humans, so researchers are seeking safer therapies, and human liver data show higher senescent macrophage signatures in diseased livers, suggesting potential relevance to people and other aging-related diseases.
A Nature Aging study identifies a distinct population of p21+ Trem2+ senescent macrophages as major drivers of inflammaging. These cells exhibit a SASP and type I interferon signaling driven in part by cytosolic mitochondrial DNA, accumulate in aging livers and in metabolic dysfunction-associated steatotic liver disease (MASLD), and are distinct from classic M1/M2 macrophages. In both mouse models and human tissue, senolytic treatment with ABT-263 reduces liver inflammation and steatosis, supporting macrophage senescence as a tractable target for aging-related liver disease.