Silicosis is a progressive fibrotic lung disease precipitated by chronic inhalation of crystalline silica. Uptake of silica particles by alveolar macrophages initiates a cascade of persistent inflammation and oxidative stress, in which reactive oxygen species (ROS) are key mediators of cellular injury and fibroproliferative remodeling. This review synthesizes the current knowledge of ROS species and signaling in silicosis and evaluates nanomaterial-based antioxidant strategies with an emphasis on cerium oxide nanoparticles (CeO2NPs). We examine the mechanistic attributes of CeO2NPs - including reversible Ce3+/Ce4+ redox cycling and enzyme-mimetic superoxide dismutase/catalase-like activities - that underpin ROS scavenging, and appraise their therapeutic potential, delivery considerations, and constraints. In parallel, we highlight opportunities and challenges associated with alternative platforms such as gold, silver, and iron-oxide nanoparticles for mitigating silica-induced oxidative injury. Among these modalities, unresolved issues include the standardization of characterization, dose‒response relationships, long-term biodistribution and clearance, immunotoxicity, interference with physiological redox signaling, and optimization of drug loading for combination therapies. Addressing these biosafety and payload questions through rigorous in vitro and in vivo studies will be essential to advance nanomaterial-enabled interventions for silicosis and related pulmonary diseases toward clinical translation.
Ban et al. (Thu,) studied this question.