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Cardiac fibrosis is a central pathological feature of many cardiovascular diseases and contributes to progressive myocardial remodeling and heart failure. Among the diverse cellular sources of activated fibroblasts, endothelial cells have emerged as a significant contributor through endothelial-to-mesenchymal transition (EndMT). During EndMT, endothelial cells lose their endothelial characteristics and acquire mesenchymal phenotypes, resulting in increased extracellular matrix deposition and tissue stiffening. Multiple pathological stimuli, including inflammatory signaling, oxidative stress, and metabolic dysregulation, activate intracellular signaling pathways that drive EndMT. In addition to these molecular mechanisms, recent studies highlight the importance of intercellular communication mediated by extracellular vesicles, particularly exosomes carrying microRNAs (miRNAs), in regulating cardiac fibrosis. Exosomal miRNAs released from endothelial cells, cardiomyocytes, and fibroblasts can modulate fibrotic signaling networks and influence EndMT progression. This review summarizes the pathological signaling pathways governing EndMT in cardiac fibrosis and discusses the emerging roles of exosomal miRNA-mediated crosstalk in cardiac remodeling. Understanding these integrated mechanisms may provide new insights into therapeutic strategies targeting cardiac fibrosis.