The cells that comprise the circulatory system not only share developmental origins but also mutually support each other’s differentiation during early embryogenesis. Although classical models attribute embryonic hematopoiesis in mammals to the yolk sac and aorta-gonad-mesonephros (AGM) region, we and others have identified the embryonic heart as a transient hematopoietic niche. A subset of endocardial cells in the outflow tract and atrioventricular canal undergo endothelial-to-hematopoietic transition (EHT) in an Nkx2-5-dependent manner, mirroring the tinman-regulated cardio-hematopoietic program in Drosophila. These hemogenic endocardial cells, enriched in the cushion region—the primordia of cardiac valves and septa—not only contribute to local hematopoiesis but also give rise to tissue macrophages that facilitate valve morphogenesis.
These findings challenge the traditional view of hematopoietic compartmentalization and establish a novel paradigm in which the heart itself contributes to hematopoietic development. Using lineage tracing and knockout mouse models, we further show that endocardial-derived macrophages persist into adulthood as tissue-resident macrophages, particularly within cardiac valves and vasculature. Functionally, these cells appear to modulate tissue homeostasis and suppress pathological fibrosis.
In summary, our study reveals that the embryonic heart acts as a local hematopoietic organ, supplying a distinct macrophage population that contributes to both cardiac morphogenesis and long-term homeostasis. These insights broaden our understanding of the interplay between hematopoiesis and cardiogenesis and suggest new avenues for investigating tissue-resident immune cell ontogeny.
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