SMAD1 and inflammation: 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.