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Hydrogels are becoming increasingly attractive for various practical applications owing to significant improvements in their fracture resistance over the past two decades. Notably, almost all existing methods for enhancing the fracture resistance of hydrogels aim to increase the fracture toughness Γ through multiscale material design. However, engineering the toughness of hydrogels at the material level often requires material-specific, complicated, or expensive synthesis processes. According to the fracture condition G = Γ , reducing the energy release rate G under given mechanical loads is an alternative way to enhance the fracture resistance. Little efforts, however, have been made to use this approach to enhance the fracture resistance of soft materials such as hydrogels so far, largely due to their highly nonlinear and deformable behavior. This paper formulates a theory for studying the fracture of monolayer and bilayer hydrogel thin films and proposes a structure-based strategy for enhancing the fracture resistance of hydrogels by constructing hydrogel films adhered to underlying stretchable substrates. Through both theoretical analysis and experimental validations, we demonstrate that the strategy exhibits several unique advantages: even a thin and compliant substrate can enhance the fracture resistance of hydrogel films by several folds, and make the fracture resistance of hydrogel films independent of the crack length and the hydrogel size – which dramatically affects the fracture behavior of monolayer hydrogels. The underlying mechanism lies in that the stretchable substrates can effectively constrain the crack opening displacements and reduce the energy release rate G for crack propagation in the hydrogel film. Moreover, the influence of experimentally-observed interfacial delamination on the fracture resistance of substrate-supported hydrogels is also investigated. The present work unveils a first-of-its-kind "structural-toughening" strategy for improving the fracture resistance of hydrogels by structurally regulating the energy release rate. [ABSTRACT FROM AUTHOR]