The present study showed that exosomal miR-1-3p is significantly increased in CLP rat models, mediates proliferation inhibition, and increases apoptosis, cell contraction, permeability, and membrane injury of endothelial cells through its target gene SERP1, leading to vascular barrier dysfunction and participating in the occurrence of sepsis-induced lung injury. The gene discussed is SERP1; the disease is Sepsis.