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A07 - Sterile inflammation and innate immunity in HFpEF

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Project summary

Low-grade inflammation induced by comorbidities is recognized to underlie HFpEF-specific remodelling. S100A8/A9 and the NLRP3 inflammasome are important contributors to sterile inflammation and splenic monocytopoeisis in the comorbidities associated with HFpEF. The projects explores the role of innate immunity in HF, evaluating whether systemic vs. cardiac deregulation of the alarmin S100A9 and NLRP3 inflammasome activity triggers HFpEF vs. HFrEF and how this influences splenic activity and potentially the cardiosplenic axis.

Graphical Abstract: In inflammatory-metabolic HFpEF, S100A8/A9 is increased in different organs (in scheme restricted to skeletal muscle and adipose tissue, as main extra-cardiac organs of interest in proposal), leading to  upregulated IL-1ß release and increased monocytopoesis in the spleen, and subsequent homing of splenic monocytes to not only the heart, but also to extra-cardiac organs including skeletal muscle and adipose tissue.


Additional group members

PhD students: Isabel Voss

Postdoc: Kathleen Pappritz





Pesce M, Duda GN, Forte G, Girao H, Raya A, Roca-Cusachs P, Sluijter JPG, Tschöpe C, Van Linthout S. Cardiac fibroblasts and mechanosensation in heart development, health and disease. Nat Rev Cardiol. 2022 Nov 14. doi: 10.1038/s41569-022-00799-2. Epub ahead of print. PMID: 36376437.

Matz I, Pappritz K, Springer J, Van Linthout S. Left ventricle- and skeletal muscle-derived fibroblasts exhibit a differential inflammatory and metabolic responsiveness to interleukin-6. Front Immunol. 2022 Jul 28;13:947267. doi: 10.3389/fimmu.2022.947267. PMID: 35967380; PMCID: PMC9366145.