Key result
Blocking von Willebrand factor worsens post-MI cardiac function despite reducing monocyte infiltration.
Spatial multiomics in a murine MI model identifies vWF as a key mediator of endocardial leukocyte infiltration, where its blockade worsens cardiac function.
Myocardial infarction (MI) continues to be a leading cause of death worldwide. Even though it is well established that the complex interplay between different cell types determines the overall healing response after MI, the precise changes in the tissue architecture are still poorly understood. In this study, we generated an integrative cellular map of the acute phase after murine MI using a combination of imaging-based transcriptomics (Molecular Cartography) and antibody-based highly multiplexed imaging (Sequential Immunofluorescence). This enabled us to evaluate cell type compositions and changes at subcellular resolution over time. We observed the recruitment of leukocytes to the infarcted heart through the endocardium and performed unbiased spatial proteomic analysis using Deep Visual Proteomics (DVP) to investigate the underlying mechanisms. DVP identified von Willebrand factor (vWF) as an upregulated mediator of inflammation 24 hours after MI, and functional blocking of vWF reduced the infiltration of C-C chemokine receptor 2 (Ccr2)-positive monocytes and worsened cardiac function after MI.
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Wünnemann et al. (2025) studied Acute myocardial infarction (murine model). Functional blocking of von Willebrand factor (vWF) was evaluated on Infiltration of Ccr2-positive monocytes and cardiac function. Functional blocking of von Willebrand factor reduced the infiltration of Ccr2-positive monocytes and worsened cardiac function after murine myocardial infarction.
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