The wound healing process involves a complex interplay of cells and molecules. Initial hemostasis occurs immediately after tissue injury, followed by overlapping phases of inflammation, proliferation, and remodeling. Vascular hyperpermeability peaks during the early phase and contributes to inflammatory responses such as hyperemia, edema, and exudate. Recently, emerging evidence has highlighted the role of vascular leakage in wound healing. This review outlines the characteristics of vascular hyperpermeability during wound repair and discusses potential mechanisms by which self-limited-but not excessive or prolonged-vascular leakage facilitates the healing process. Transient vascular hyperpermeability or localized intratissue bleeding during the inflammatory phase permits the entry of plasma-derived molecules into the wound. Extravasated fibrinogen, growth factors, and cells (e.g., platelets and red blood cells) promote healing, at least in part, by enhancing angiogenesis and reducing inflammation. Several substances and wound care products have demonstrated this effect in supporting wound repair. By contrast, excessive or chronic vascular leakage-such as that resulting from ineffective angiogenesis-impairs healing through various detrimental mechanisms, including chronic inflammation. Interestingly, although chronic vascular hyperpermeability contributes to delayed healing in diabetic foot ulcers, temporally controlled enhancement of vascular leakage may help restore the repair process by promoting effective angiogenesis and reducing inflammation. Together, these findings offer new insights into the role of vascular leakage in wound repair and suggest potential therapeutic strategies to enhance wound healing.