Aged mice lacking an immune protein had less heart dysfunction
Experiments in isolated hearts from 21-month-old male mice found better recovery without the protein after flow through the heart stopped and restarted.
Edited by Boris Djordjevic · AgingResearch.News
In an animal experiment, researchers studied male C57BL/6 mice aged 21 months, using 3-month-old mice as young controls. They compared mice with and without AIM2, a protein involved in an inflammation-triggering complex. They tested isolated hearts by stopping and restarting fluid flow through them.
In aged mice, hearts lacking AIM2 recovered more of their ability to generate pressure after flow resumed. They also had lower baseline levels of signals linked to inflammation and inflammatory cell death. AIM2 levels rose in aging hearts. Its absence did not alter age-related heart enlargement, scarring, lifespan or markers of senescence, a state in which cells stop dividing.
Why it matters
The work points to an inflammation-related pathway for investigating why aging hearts become more vulnerable to damage when circulation is interrupted and restored.
Caveats
Heart function was tested in isolated hearts, so these functional results do not establish benefits in living animals or people. The mouse experiments used males only.
The paper
Universidade de São Paulo
Clinical Science, Oct 22, 2026, Open access
