SAN fibroblasts presented robust myofibroblast differentiation and fibronectin secretion in HF human hearts, and POSTN-positive fibrotic islands increased in human HF SAN, which led to intranodal structural barriers interrupting normal automaticity and conduction, whereas molecular and protein markers were distinguished from RA fibroblasts in non-HF SAN fibroblasts, indicating these proteomic datasets could be used to identify novel SAN fibroblast-specific targets to develop antifibrotic strategies [109]. This evidence concerns the gene FN1 and hydrops fetalis.