Regarding the interactions between fibroblasts and other cell types, potential pathways such as Cxcl12-Ackr3, Ptn-Ncl, and Mdk-Lrp1 may represent promising targets to block the primary communication between the C1 Postn + Fibroblasts and EndoCs, ECs, and macrophages, offering meaningful suggestions for therapeutic strategies to address myocardial fibrosis after MI. This evidence concerns the gene MDK and myocardial infarction.