A Triple‐Functional Nanoplatform for Oxidative Stress‐Driven Pressure Ulcer Therapy

Pressure ulcers (PUs) are chronic wounds driven by persistent inflammation, oxidative stress, impaired angiogenesis, and delayed remodeling, yet current treatments remain suboptimal. Here, we developed a novel nanocomposite (CCH) by loading cerium oxide (CeO 2 ) and curcumin into hollow mesoporous silica nanoparticles (HMSN). CCH exhibited well‐defined spherical morphology, favorable particle size, and pH‐dependent drug release. Mechanistically, CCH possessed potent superoxide dismutase (SOD)‐ and catalase (CAT)‐mimetic activities, effectively scavenging reactive oxygen species. In vitro, CCH was efficiently internalized by HUVECs, showed excellent biocompatibility up to 100 μg/mL, protected HUVECs from oxidative damage by reducing intracellular ROS and restoring VEGF secretion, and induced anti‐inflammatory M2 macrophage polarization. In a mouse model of pressure ulcer, topical CCH application significantly accelerated wound closure, enhanced re‐epithelialization and granulation tissue formation, reduced systemic CRP and PCT levels, and improved scar prognosis, associated with increased VEGF expression and CD31‐positive vascularization, along with organized collagen deposition. Collectively, CCH integrates antioxidant, anti‐inflammatory, pro‐angiogenic, and tissue‐remodeling functions into a single nanoplatform, effectively addressing key pathological features of PUs. Thus, CCH represents a promising and safe candidate for chronic wound management.