Skin wound healing is a multifaceted biological process that encompasses critical stages such as inflammation modulation, angiogenesis, cellular proliferation, and extracellular matrix (ECM) remodeling, including the restructuring of collagen [1,2]. The synchronized regulation of angiogenesis and collagen metabolism constitutes the pivotal link in wound healing. CD31 (platelet-endothelial cell adhesion molecule), an endothelial cell marker, plays a crucial role in determining the maturity and functional integrity of neovascularization through its expression levels [3,4]. Vascular endothelial growth factor (VEGFa) not only facilitates the migration and tube formation of endothelial cells but also stimulates fibroblasts to secrete type III collagen via paracrine signaling, thereby optimizing ECM structure [5,6]. Notably, type III collagen, characterized by its fine fiber diameter and orderly arrangement, inhibits excessive fibrosis and promotes epithelial regeneration during early wound repair. Its content exhibits a significant negative correlation with scar formation [7]. However, chronic wounds, such as diabetic foot ulcers and deep burns, often result in delayed healing and tissue fibrosis due to impaired angiogenesis, imbalanced collagen metabolism, and persistent inflammation [8]. The global incidence of these conditions is rising annually, posing a significant challenge in clinical treatment [9]. While traditional therapies, including hydrogel dressings, recombinant growth factors, and antibiotics, can promote acute wound repair through local moisturizing and anti-infection properties, they encounter limitations such as insufficient vascularization, abnormal ECM remodeling, and low drug delivery efficiency in chronic wounds [10]. Consequently, there is an urgent need to develop new biomaterials that possess both pro-angiogenic and collagen-regulating functions.

In recent years, significant advancements in nanotechnology have provided novel approaches for wound repair [11]. Metal-Organic Frameworks (MOFs) have demonstrated considerable potential in tissue engineering due to their tunable pore structure, high drug loading capacity, and catalytic activity [12,13]. Prussian Blue (PB), a classical peroxide-like nanomaterial, not only mitigates oxidative stress injury by scavenging reactive oxygen species (ROS) but also modulates macrophage polarization to improve the inflammatory microenvironment [14,15]. However, unmodified PB nanoparticles tend to aggregate due to uneven surface charge, leading to reduced bioavailability and lack of targeting specificity [16]. To address this issue, Bovine Serum Albumin (BSA) modification has been extensively employed to enhance colloidal stability via hydrophobic interactions and covalent cross-linking [17], leveraging BSA's natural receptor-mediated properties to improve cellular uptake efficiency [18].

In this study, we modified Prussian blue with bovine serum albumin (BSA) to enhance its therapeutic efficacy. We subsequently characterized the morphology and functionality of BSA@PB. To evaluate its performance in a skin injury model, we induced full-thickness skin defects on the dorsal region of mice and observed that BSA@PB significantly accelerated wound healing in vivo. Moreover, BSA@PB demonstrated the capability to promote collagen synthesis and angiogenesis within the injured area. These findings indicate that BSA@PB has potential as an effective modality for promoting wound healing through enhanced angiogenesis at the site of injury. By integrating nanomaterials engineering and molecular biology methodologies, this study aims to provide innovative strategies for treating chronic wounds while advancing our understanding of nano-biology interactions.