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Myocardial fibrosis is a common pathophysiological process observed in various cardiac diseases and cardiac aging, characterized by excessive accumulation of extracellular matrix proteins in the cardiac interstitium. This process is highly heterogeneous and dynamic, depending on the underlying cardiac pathology and disease stage, and represents a key pathological basis for the development and progression of heart failure. Thrombospondin-2 (TSP-2), a critical extracellular matrix regulatory protein, exhibits complex dual roles in different disease contexts and stages, exerting both cardioprotective and potentially pathological effects. Recent studies have demonstrated that TSP-2 is involved in the pathogenesis of heart failure and may regulate myocardial fibrosis through modulation of extracellular matrix remodeling and related signaling pathways. This review summarizes the regulatory roles of TSP-2 in myocardial fibrosis under various cardiac disease conditions and discusses its potential molecular mechanisms. By integrating current studies, this review provides new insights into the regulatory network of myocardial fibrosis and highlights the potential of TSP-2 as a therapeutic target. However, further mechanistic and translational studies are required to validate the precise role and clinical applicability of TSP-2 in cardiac fibrosis.