# Balancing act: how Apelin tunes vascular and haemogenic identities

**Authors:** Rui Monteiro

PMC · DOI: 10.1038/s44319-026-00696-6 · EMBO Reports · 2026-01-26

## TL;DR

Apelin signaling helps balance blood vessel development and the formation of blood stem cells during embryonic development.

## Contribution

Apelin signaling is shown to indirectly regulate haemogenic endothelial cell fate independently of Notch, BMP, or Wnt.

## Key findings

- Apelin signaling limits arterial endothelial cells from becoming haemogenic.
- Higher haematopoietic stem and progenitor cell numbers result from increased haemogenic endothelial conversion.
- Apelin acts as a rheostat during a critical developmental window.

## Abstract

Haematopoietic stem and progenitor cells (HSPCs) maintain haematopoiesis throughout life. Their formation occurs early in embryonic development and is regulated by many intrinsic and extrinsic factors that delicately balance the need to maintain a vascular network with the need to generate HSPCs de novo. Most extrinsic factors such as BMP and Notch act instructively in haemogenic endothelial cells to induce HSPC fates. A new study by Eberlein et al (2025) identifies a key role for Apelin signalling acting indirectly by limiting the number of arterial endothelial cells that become haemogenic, independently of Notch, BMP or Wnt signalling (Eberlein et al, 2025). Arterial endothelial cells that do not respond to Apelin more frequently convert to the haemogenic endothelial cell fate, giving rise to higher numbers of haematopoietic stem and progenitor cells in the embryo that persist into adulthood. This work highlights a critical temporal window where Apelin functions as a rheostat, balancing angiogenesis, vascular maintenance and haematopoiesis.

New research in EMBO Reports identifies a function for Apelin signaling in balancing angiogenesis, vascular maintenance and haematopoiesis.

## Full-text entities

- **Genes:** APLN (apelin) [NCBI Gene 8862] {aka APEL, XNPEP2}

## Full text

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## Figures

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## References

1 references — full list in the complete paper: https://tomesphere.com/paper/PMC12936074/full.md

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Source: https://tomesphere.com/paper/PMC12936074