Deleting an immune-cell receptor reduces fat inflammation in mice
In male and female mice studied across aging, lacking the mineralocorticoid receptor in macrophages prevented inflammatory cell expansion and improved fat tissue remodeling.
Limit: Fat inflammation was measured; cardiovascular and metabolic function were not measured
Edited by Boris Djordjevic · AgingResearch.News
In an experiment in male and female mice across aging, researchers examined how the mineralocorticoid receptor in macrophages, a type of immune cell, affects fat around internal organs. They analyzed gene activity in fat-tissue macrophages from mice with and without this receptor in those cells. The team also analyzed published sequencing data from aging human abdominal white fat tissue.
In aging mice, a specific macrophage subpopulation expanded over time. Lacking the receptor in macrophages prevented this expansion and prevented the activation of genes linked to age-related inflammation in these cells. The deficiency also reduced inflammatory activation of fat cells and improved tissue remodeling, including cellular senescence, a state in which cells stop dividing, and fibrosis, which is tissue scarring. In the human fat data, this macrophage subpopulation was similarly expanded with age and showed higher receptor expression.
Why it matters
Inflammation in aging fat tissue contributes to metabolic problems and cardiovascular disease. The findings suggest that this receptor’s signaling in macrophages may be a target for limiting problems with metabolism and cardiovascular function.
Caveats
The experimental findings came from genetically altered mice, while the human results were limited to an analysis of published sequencing data. The supplied report was an ESC Congress 2026 abstract.
The paper
Macrophage mineralocorticoid receptor drives inflammaging in adipose tissue
Medizinische Hochschule Hannover
ESC Congress 2026 Abstract, Oct 26, 2026, Open access
Presented at ESC Congress 2026
