A proposed model of enhanced clot retraction in the presence of limited fibrinolysis. The studies presented here are consistent with the hypothesis that low concentrations of tPA-mediated plasmin formation trigger limited fibrinolysis, which in turn makes the fibrin network more amenable to compaction by platelet contractile forces. During blood clot development, platelets interact with fibrin polymers (red), with contractile force generated internally within the platelet transmitted to the external fibrin clot, resulting in retraction and fibrin clot shrinkage (A→B). The level of platelet-mediated clot shrinkage is balanced by the rigidity of the 3D fibrin network, which opposes platelet-mediated contractile forces (blue arrows). In the presence of limited tPA-mediated fibrinolysis, clot rigidity is reduced in a localized fashion (right), releasing forces opposing platelet contractility, resulting in increased fibrin clot retraction, via localized release of tension (B).