Published on: Jan 02, 2026
The Faculty of Medicine at The Chinese University of Hong Kong (CU Medicine) has made a world-first discovery demonstrating that CD4⁺ FOXP3⁺ regulatory T cells (CD4⁺ Treg cells) precisely regulate MRG15, a key factor in neonatal cardiac regeneration. The team also uncovered the mechanism by which these immune cells promote heart development and repair, identifying a novel therapeutic target for cardiac regenerative medicine. Published in the leading cardiovascular journal Circulation, the findings offer new hope for treating myocardial infarction and heart failure in China and worldwide.
Unlike adult hearts, which lack the ability to regenerate damaged cardiomyocytes, neonatal hearts possess a transient capacity for repair that rapidly declines with age. This loss of regenerative potential contributes significantly to the global burden of cardiovascular diseases, which cause nearly 20 million deaths annually worldwide.
Building on earlier work, Professor Kathy Lui Oi-lan and her team showed that cardiac injury in neonates activates CD4⁺ Treg cells, which secrete factors that directly stimulate cardiomyocyte proliferation. After six years of further research, the team identified MRG15—a chromatin-modifying protein highly expressed in neonatal cardiomyocytes as a critical mediator of this process.
Using gene knockout and reactivation models, the researchers demonstrated that loss of either CD4⁺ Treg cells or MRG15 markedly impairs cardiac regeneration, while restoring MRG15 rescues regenerative function even in the absence of Treg cells. Mechanistic studies revealed that neonatal CD4⁺ Treg cells induce MRG15 to form a transcriptional complex that activates cyclin D1, driving cardiomyocyte proliferation and repair. This regenerative capacity is absent in adult Treg cells.
The study redefines CD4⁺ Treg cells as not only immune regulators but also key facilitators of heart repair. The researchers now aim to translate these findings into immune cell–based therapies for myocardial infarction and heart failure.
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