Abstract:Septic acute lung injury（SALI）is one of the common complications of sepsis，with a high incidence and closely related to the high mortality of patients in the intensive care unit. The pathophysiological mechanism of SALI is complex and involves multiple aspects such as dysfunction of the pulmonary vascular endothelial barrier. Endothelial glycocalyx（EG），a polysaccharide-protein complex covering the surface of vascular endothelial cells，plays a key role in maintaining vascular integrity，regulating inflammatory responses and coagulation functions. Recent studies have demonstrated that the damage of EG plays an important role in the occurrence and progression of SALI. This article reviews the structural and functional basis of EG，and focuses on discussing the molecular mechanism of EG damage in sepsis and its role in SALI，aiming to provide a theoretical basis for the exploration of therapeutic targets and the development of related drugs for SALI.