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. 2021 Oct 6;12:701721. doi: 10.3389/fimmu.2021.701721

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Copyright © 2021 Mollenhauer, Bokredenghel, Geißen, Klinke, Morstadt, Torun, Strauch, Schumacher, Maass, Konradi, Peters, Berghausen, Vantler, Rosenkranz, Mehrkens, Braumann, Nettersheim, Hof, Simsekyilmaz, Winkels, Rudolph, Baldus, Adam and Freyhaus

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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Schematic overview of PMN activation and fibrotic remodeling in Stamp2^-/- mice after I/R. Stamp2 deficiency results in NmRal-mediated proinflammatory NF-κB activation (11, 15) which subsequently induces enchanced myocardial PMN infiltration after I/R injury. PMN degranulation and MPO secretion are elevated in Stamp2^-/- PMN, thereby activating the p38-MAPK pathway and inducing fibroblast-to-myofibroblast transdifferentiation. In turn, enchanced collagen deposition promotes maladaptive structural remodeling finally leading to loss of LV function. PMN: polymorphonuclear neutrophils, Stamp2: six transmembrane protein of prostate 2, NF-κB: nuclear factor ‘kappa-light-chain-enchancer’ of activated B-cells, NmRal: NmrA-like family domain- containing protein 1, MPO: myeloperoxidase, p-p38/p38: phosphor/ p38 MAP kinase. Figures were produced using Servier Medical Art (http://www.servier.com/).