The formation of neutrophil extracellular traps (NETs) is a novel way for neutrophils to perform organismal protective functions essential for protecting the host against infections. Nevertheless, an increasing amount of data shows that uncontrolled or excessive formation of NETs in the body leads to inflammation and thrombosis. Many serious human diseases, such as sepsis, stroke, cancer, and autoimmune diseases, are associated with thrombosis, and inhibiting its formation is essential to prevent the development of many inflammatory and thrombotic diseases. With deeper research, it has been found that there is a complex interaction between NETs and platelets: platelets activate neutrophils to form NETs, while NET components enhance platelet aggregation and activation. This self-perpetuating vicious cycle between them mediates pathological processes such as inflammation, coagulation, and thrombosis. A deeper comprehension of the underlying molecular mechanisms between them promises to be a new target for thrombotic diseases. In this review, we concentrate on a summary of NET formation and its mechanisms of action. Providing a thorough summary of how neutrophils are activated by platelets to form NETs, how NETs cause platelet activation, and how this close interaction during inflammatory events affects the course of the disease, with the aim of providing fresh targets and ideas for thrombotic disease clinical prevention and therapy.