Exercise may protect hearts partly via a brown fat molecule in mice
In mice with diabetic heart disease, removing brown fat blunted the protective effects of voluntary exercise by causing a shortage of the signaling molecule maresin 2.
Limit: NLRP3 inflammasome and cytokine levels served as stand-ins; heart function was not measured
Edited by Boris Djordjevic · AgingResearch.News
In an experiment in mice, researchers gave animals a high-fat diet and streptozotocin to model diabetic heart disease and heart failure, followed by voluntary exercise. They surgically removed brown fat from between the shoulder blades of some animals. Removing this fat markedly blunted the heart-protecting effects of exercise. Exercise promoted brown fat to release maresin 2, a signaling molecule, into the bloodstream and heart tissue. Supplying maresin 2 to the mice expanded a group of heart immune cells and suppressed both an inflammatory complex called the NLRP3 inflammasome and the subsequent release of two inflammatory proteins, IL-1β and IL-18.
In both mice and mouse immune cells grown in the lab, deleting the gene for Trem2, a cell-surface protein, abolished this anti-inflammatory effect. Depleting Trem2 also reversed the protective effects of exercise against diabetic heart disease in the mice.
Why it matters
Heart failure with preserved ejection fraction is a common age-related condition that remains largely resistant to medical treatments. Uncovering how exercise stimulates fat-derived signals to ease cardiac inflammation may guide therapeutic approaches for heart disease tied to metabolic dysfunction.
Caveats
The experiments were conducted in mice and lab-grown mouse cells rather than people, so the findings may not translate to human heart disease. The report was also presented as a conference abstract that has not yet undergone full peer review.
The paper
West China Hospital; General Hospital of the Western Theater Command
ESC Congress 2026 Abstract, Oct 26, 2026
Presented at ESC Congress 2026
