Figure 1.

Overview of the pathogenesis of sepsis, which involves several pathophysiological processes, such as endothelial injury, breakdown of the endothelial barrier, immune thrombosis, and disseminated intravascular coagulation (DIC). Various factors contribute to the development of sepsis, including damage-associated molecular patterns (DAMPs), interleukins (ILs), Toll-like receptor 4 (TLR4), and tumor necrosis factor-alpha (TNF-α). The interplay of these factors in the pathogenesis of sepsis leads to the activation of coagulation pathways and inflammatory responses, and organ and organ dysfunction.