Fat tissue signals linked to immune activity in mouse vessels
Cell analysis in aging mice and mice with diet-induced obesity linked signals from fat tissue to a shared immune response across four organs.
Limit: Direct cell-to-cell communication was not measured, only inferred computationally from gene expression
Edited by Boris Djordjevic · AgingResearch.News
In an experiment in mice exposed to natural aging or diet-induced obesity, researchers analyzed endothelial cells, which line blood vessels, from fat tissue, heart, skeletal muscle and liver. They measured gene activity in individual cells and used computer analysis to infer communication between cells.
Aging changed gene activity differently across organs but increased interferon signaling, part of the immune response, in all four. Obesity produced organ-specific patterns of gene activity related to fat metabolism and inflammation. The computer analysis linked signals from macrophages, a type of immune cell in fat tissue, to interferon activation in vessel-lining cells. The implicated signal was tumor necrosis factor, an immune signaling protein. Cells with high interferon activity formed clusters in every organ. In heart and skeletal muscle, these clusters promoted anti-inflammatory behavior in macrophages.
Why it matters
Blood vessel disease progresses differently across organs despite bodywide stress from aging and obesity. The work addresses how inflammatory signals may contribute to those differences.
Caveats
Cell-to-cell communication was inferred computationally, so those links alone do not establish cause and effect. The findings came from mice and were reported in a conference abstract.
The paper
Single-cell analysis reveals inter-organ endothelial crosstalk in aging and obesity
Chiba University Graduate School of Medicine
ESC Congress 2026 Abstract, Oct 26, 2026
Presented at ESC Congress 2026
