Hemostasis, the process by which platelets form a clot to halt blood loss following vessel damage, must be tightly regulated to ensure that a clot forms quickly to prevent excess blood loss without restricting blood flow to the rest of the body. Conceptually, a sophisticated biological control system is responsible for maintaining this tight regulation, realized physiologically by a complex set of interactions between many different molecules both inside and outside the platelet. Precisely how all the individual components work together to maintain this balance has been difficult to understand using traditional experimental methods alone—quantitative models are required.

In this work, we develop an engineering control system-based model of the process of hemostasis, organizing essential components in terms of their respective control system functions, i.e. as sensors, controllers, actuators, and the controlled process. By organizing key molecular interactions according to their function within the hemostatic control system, and using known biological characteristics to model them as inter-connected units, we have created a model that represents the process of hemostasis in terms of it's effectiveness at controlling blood loss following vessel injury. Our model includes mechanistic details within the framework of the overall system properties; this approach enables us to identify the molecular source of system malfunctions and design corrective action based on the desired system properties. We show how different components of the hemostatic system affect overall responses to vessel injury, and how we can use the model to formulate and test hypotheses regarding the causes and effects of different pathological conditions.