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<p>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.</p>

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Spatial multiomics of acute myocardial infarction reveals immune cell infiltration through the endocardium

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年10月3日

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  • Florian Wünnemann,
  • Florian Sicklinger,
  • Kresimir Bestak,
  • Jose Nimo,
  • Tobias Thiemann,
  • Junedh M. Amrute,
  • Mathias Nordbeck,
  • Niklas Hartmann,
  • Miguel A. Ibarra-Arellano,
  • Jovan Tanevski,
  • Margot Chazotte,
  • Clara Heine,
  • Norbert Frey,
  • Kory J. Lavine,
  • Fabian Coscia,
  • Julio Saez-Rodriguez,
  • Florian Leuschner,
  • Denis Schapiro

摘要

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.