Study on deformation mechanism of fibrin protofibril and fiber using hierarchical network model

Abstract Fibrin fibers represent the secondary structural units within the fibrin network, and their complex deformation mechanisms directly govern the unique mechanical behavior of blood clots. A hierarchical node–pair network model was developed to elucidate the microscale deformation mechanisms of fibrin protofibrils and fibers under tension. This model abstracts microscale structural interactions into distinct bonding types characterized by specific force–extension relationships. Simulation results reveal that the tensile response of an individual protofibril exhibits four distinct stages and sequential unfolding of coiled–coils dominating the unfolding stage. Upon lateral assembly into fibrin fibers, the incorporation of crosslinks in the α C regions introduces localized structural constraints that inhibit the orderly unfolding of coiled–coils. This non–sequential deformation mechanism blurs the boundary between the unfolding and stiffening stages, giving rise to a bilinear force–strain response characterized by a slope transition. Finally, the crosslink density between protofibrils significantly influences the overall deformation mechanism of fibrin fibers. At low crosslink densities, fibers preserve the sequential coiled–coils unfolding behavior of individual protofibrils and exhibit a higher peak force. As the crosslink density increases, non–sequential unfolding mechanism becomes dominant, resulting in a non–monotonic trend in peak force–initially decreasing and then increasing. These findings provide mechanistic insight into fibrin fiber deformation and may also offer a basis for future extensions toward three–dimensional fiber architectures and microscale–to–macroscale constitutive modeling.