The preservation of physiological BMP4 concentrations in TCRM hearts after 14-D10-2 treatment (Fig. 4o) and the elevated SMAD1/5/9 phosphorylation in cardiac fibroblasts (Extended Data Fig. 4i,j) underscore that antibody-mediated restoration of BMP4 availability and BMPR signaling in the cardiac microenvironment efficiently counteracts immune cell and fibroblast activation in the course of acute myocardial inflammation. This evidence concerns the gene BMP4 and inflammatory response.