Chronic subdural hematoma (CSDH) is a collection of blood, blood clots and their degradation products, encapsulated by membrane and located within dural border cell layer. Pathophysiological processes such as inflammatory responses within hematoma cavity, coagulation abnormalities, and abnormalities in neovascularization play significant roles in CSDH development. High mobility group box 1 (HMGB1) can mediate processes such as inflammation, angiogenesis, and hemostasis, while thrombomodulin (TM) can bind with HMGB1 and rely on thrombin to degrade HMGB1. Current research has confirmed that the expressions of TM, HMGB1, and their downstream related factors are abnormally increased in the hematoma fluid of CSDH; however, the role of TM-thrombin-HMGB1 pathway in CSDH development is not fully clear. This article reviews the role of TM-thrombin-HMGB1 pathway in CSDH development, aiming to provide some references for pathogenesis and new therapeutic targets of CSDH.

Traumatic brain injury(TBI)is a multifaceted disease with a complex pathogenesis for which there are currently no effective therapeutic interventions.Research has shown that bone marrow mesenchymal stem cell-derived extracellular vesicles(BMSC-EVs)may play a therapeutic role in TBI.They attenuate neuroinflammatory responses at the site of the lesion and promote neurovascular regeneration.However,the exact mechanisms underlying their actions are not fully understood.This article aims to review the current state of research on the therapeutic mechanisms of BMSC-EVs in TBI.It also aims to discuss possible future research directions and potential clinical applications of BMSC-EVs.