Acute wounds present a significant clinical challenge due to delayed healing, which is often exacerbated by elevated levels of reactive oxygen species (ROS). These high ROS concentrations hinder the natural healing process, leading to prolonged recovery and increased risk of complications. W-GA nanodots, synthesized via a simple coordination method, have emerged as promising solutions, demonstrating multifunctional enzymatic activity that effectively scavenges ROS. To explore the underlying mechanisms of ROS-induced oxidative stress, we conducted RNA sequencing on macrophages exposed to HO. The results revealed significant regulation of key stress response pathways, including substantial upregulation of the "p53 signaling pathway" and the "HIF-1 signaling pathway," both of which are essential for cellular adaptation to oxidative stress. By alleviating oxidative stress, W-GA nanodots not only accelerate wound repair but also improve overall healing outcomes. Notably, RNA sequencing of animal tissue samples revealed that W-GA nanodots activate the "Wnt signaling pathway," further promoting wound healing. These findings underscore the potential of W-GA nanodots as a novel therapeutic strategy for enhancing wound healing and treating oxidative stress-related conditions, positioning them as promising candidates for future clinical applications in wound care and inflammatory diseases.
