In summary, our study has uncovered that in the DF ulcer microenvironment, EVs in the wound fluid appear to inhibit angiogenesis and wound healing, which is at least partially mediated by increased expression of antiangiogenic miR-205-5p and miR-195-5p, which in turn suppress the expression of the key proangiogenic factor VEGFA. The gene discussed is VEGFA; the disease is ulcer disease.