Аннотация:Traumatic brain injury (TBI) is one of the leading causes of mortality and disability amongyoung and middle-aged individuals. Adequate and timely diagnosis of primary brain injuries, as wellas the prompt prevention and treatment of secondary injury mechanisms, significantly determine thepotential for reducing mortality and severe disabling consequences. Therefore, it is crucial to haveobjective markers that indicate the severity of the injury. A number of molecular factors—proteins andmetabolites—detected in the blood immediately after trauma and associated with the developmentand severity of TBI can serve in this role. TBI is a heterogeneous condition with respect to its etiology,clinical form, and genesis, being accompanied by brain cell damage and disruption of blood–brainbarrier permeability. Two oppositely directed flows of substances and signals are observed: one isthe flow of metabolites, proteins, and nucleic acids from damaged brain cells into the bloodstreamthrough the damaged blood–brain barrier; the other is the infiltration of immune cells (neutrophilsand macrophages) and serological proteins. Both flows aggravate brain tissue damage after TBI.Therefore, it is extremely important to study the key signaling events that regulate these flows andrepair the damaged tissues, as well as to enhance the effectiveness of treatments for patients after TBI.