Immune cell group helps repair hearts in newborn mice
Experiments in newborn mice found that removing these cells reduced heart muscle cell multiplication and worsened inflammation and scarring after heart attacks.
Limit: Heart repair was assessed by cell proliferation and fibrosis; heart function was not measured
Edited by Boris Djordjevic · AgingResearch.News
In experiments in newborn and adult mice, researchers compared heart macrophages, a type of immune cell, ten days after heart attacks. They identified a group more common in newborn hearts marked by high levels of the protein S100A8.
This group expanded in newborn hearts as neutrophils, another type of immune cell, cleared more quickly. Adult hearts instead retained neutrophils and ongoing inflammation. Genetically removing the S100A8-marked macrophages impaired heart regeneration in newborn mice. Heart muscle cells multiplied less, while inflammation and scarring worsened. Further tests in cells grown in the lab and in mice found that these macrophages caused neutrophils to undergo programmed cell death. The researchers concluded that the macrophages helped coordinate the resolution of inflammation, heart muscle cell multiplication and new blood vessel growth.
Why it matters
Adult mammalian hearts have limited ability to replace lost muscle after a heart attack. Understanding the repair capacity present early in life may guide efforts to improve recovery.
Caveats
These experiments did not establish whether targeting the cells would improve heart repair in adult mice or humans. The congress abstract did not give sample sizes.
The paper
National Taiwan University College of Medicine
ESC Congress 2026 Abstract, Oct 26, 2026
Presented at ESC Congress 2026
