Influence of ischaemic cardiomyopathy on haematopoiesis (A7)

The relationship between systemic leukocytosis and heart failure progression after myocardial infarction is well documented; however, the underlying mechanisms are still unknown. We want to understand bone marrow remodelling post myocardial infarction and how this contributes to disease-promoting myelopoiesis and thrombopoiesis.

Haematopoiesis in myocardial infarction

The causal relationship between systemic leukocytosis and heart failure progression following myocardial infarction is well documented, and clinical studies show that leucocytosis is associated with increased cardiovascular mortality. Preliminary data reveal that bone marrow (BM) angiogenesis post myocardial infarction (MI) is a critical driver of enhanced haematopoiesis regulating the output and phenotype of disease-promoting leukocytes.

Rationale and aims

We aim to better understand how heart failure modulates the bone marrow vasculature, resulting in accelerated monocyte, neutrophil production and thrombopoiesis.


We will use high-end multi-colour fluorescence approaches such as intravital and light-sheet fluorescence microscopy, multicolour flow cytometry and single-cell sequencing to gain new insights into the mechanisms underlying bone marrow remodelling post myocardial infarction.


Significance and outlook

We expect that this approach will enable us to identify intervention targets to stop the detrimental feed-forward loop of MI-triggered haematopoiesis.


Portraitfoto von Dr. David Stegner

Prof. Dr. rer. nat.
David Stegner

Leader of the CRC project A7

+49 931 31-80419


Medizinische Klinik und Poliklinik I, Universitätsklinikum Würzburg, Zentrum für Innere Medizin (ZIM), Oberdürrbacher Straße 6, Haus A3, 97080 Würzburg, Deutschland 

Deutsches Zentrum für Herzinsuffizienz Würzburg | Comprehensive Heart Failure Center | Am Schwarzenberg 15 | Haus A15 | 97078 Würzburg