A Northwestern Medicine study reveals a key difference in how macrophages help repair hearts in newborns versus adults after a heart attack. Newborns can regenerate heart tissue thanks to a process called efferocytosis, where macrophages recognize and eat dying cells, triggering the production of thromboxane, a signaling molecule that prompts heart muscle cell division. Adults, however, produce less thromboxane, leading to weaker repair signals and scar tissue buildup.
Northwestern UniversityFeb 11 2025 Newborns with heart complications can rely on their newly developed immune systems to regenerate cardiac tissues, but adults aren't so lucky. After a heart attack, most adults struggle to regenerate healthy heart tissue, leading to scar-tissue buildup and, often, heart failure.
In newborns, macrophages perform a process called efferocytosis, which recognizes and eats dying cells. This process triggers the production of a bioactive lipid called thromboxane, signaling nearby heart muscle cells to divide, and allowing the heart to regenerate damaged heart muscle, the study found. In adults, macrophages produce much less thromboxane, leading to a weaker repair signal.
HEART REPAIR IMMUNE SYSTEM Macrophages REGENERATION AGE
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