Platelets are central regulators of fibrinolysis, as they harbor and interact with a wide array of fibrinolytic components and related proteins, allowing them to either suppress or promote fibrin removal. Traditionally, platelets are recognized for their role in enhancing fibrinolytic resistance, ensuring the stability of the hemostatic plug by preventing its premature dissolution. This is achieved predominantly through mechanisms such as clot retraction, the substantial release of plasminogen activator inhibitor-1, and the amplification of thrombin generation, which activates multiple antifibrinolytic pathways. Emerging evidence, however, highlights the profibrinolytic properties of platelets, which appear to facilitate clot retraction during the early stages of hemostasis and may contribute to fibrin breakdown in the later, lytic phase of the process. Furthermore, the activation of fibrinolysis itself exerts profound and, at times, paradoxical effects on platelet functionality, underscoring the bidirectional and intricate crosstalk between these systems. This chapter delves into the current understanding of the multifaceted interactions between platelets and fibrinolysis and examines their implications for physiological and pathological hemostasis.