@article{doi-e22fef36dddb9e1b,
  title = {Modulation of bone marrow haematopoietic stem cell activity as a therapeutic strategy after myocardial infarction: a preclinical study},
  author = {Jasmin Rettkowski and Mari Carmen Romero-Mulero and Indranil Singh and Carolin Wadle and Jan Wrobel and Diana Chiang and Natalie Hoppe and Julian Mess and Katharina Schönberger and Maria-Eleni Lalioti and Karin Jäcklein and Beatriz SilvaRego and Timon Bühler and Noémie Karabacz and Mirijam Egg and Helen Demollin and Nadine Obier and Yu Wei Zhang and Claus Jülicher and Anne Hetkamp and Martin Czerny and Michael-Jason Jones and Hana Seung and Ritika Jain and Constantin von zur Mühlen and Alexander Maier and Achim Lother and Ingo Hilgendorf and Peter van Galen and Antonia Kreso and Dirk Westermann and Alejo E. Rodriguez-Fraticelli and Timo Heidt and Nina Cabezas-Wallscheid},
  journal = {Nature Cell Biology},
  year = {2025},
  volume = {27},
  number = {4},
  pages = {591-604},
  doi = {10.1038/s41556-025-01639-4},
  abstract = {Abstract Myocardial infarction (MI) is a major global health concern. Although myeloid cells are crucial for tissue repair in emergency haematopoiesis after MI, excessive myelopoiesis can exacerbate scarring and impair cardiac function. Bone marrow (BM) haematopoietic stem cells (HSCs) have the unique capability to replenish the haematopoietic system, but their role in emergency haematopoiesis after MI has not yet been established. Here we collected human sternal BM samples from over 150 cardiac surgery patients, selecting 49 with preserved cardiac function. We show that MI causes detrimental transcriptional and functional changes in human BM HSCs. Lineage tracing experiments suggest that HSCs are contributors of pro-inflammatory myeloid cells infiltrating cardiac tissue after MI. Therapeutically, enforcing HSC quiescence with the vitamin A metabolite 4-oxo-retinoic acid dampens inflammatory myelopoiesis, thereby modulating tissue remodelling and preserving long-term cardiac function after MI.}
}