The Role of Protein Ubiquitination in the Onset and Progression of Sepsis

Sepsis is a life-threatening disease characterized by a dysregulated host response to infection, with complex pathophysiological mechanisms. As an important post-translational modification, protein ubiquitination exhibits multiple non-traditional functions in sepsis beyond its conventional role in protein degradation. Regulating the network of inflammatory cytokines, the dynamic balance of immune cells, and organ-specific protective pathways is deeply involved in the pathological process of sepsis. This review focuses on the non-traditional roles of protein ubiquitination in sepsis, including its regulation of the inflammatory response, immune cell functions, and organ protection. It systematically summarizes the regulatory mechanisms of ubiquitination in the non-degradative activation of the NF-κB signaling pathway, the dynamic assembly of the NLRP3 inflammasome, the reprogramming of macrophage polarization, and the injuries of organs such as the heart, liver, and lungs. The aim is to provide new insights into the understanding and treatment of sepsis.