Roles on cuproptosis in respiratory diseases

Cuproptosis is a mitochondria-dependent form of programmed cell death characterized by copper ion accumulation, which triggers the aggregation of lipoylated proteins and the destabilization of iron-sulfur cluster proteins, leading to metabolic disruption and subsequent cell death. Its mechanism is distinct from established programmed cell death pathways such as apoptosis and ferroptosis. Because respiratory tissues rely heavily on oxidative metabolism, they are particularly sensitive to perturbations in copper homeostasis. Emerging evidence indicates that copper metabolic dysregulation is widely present in various respiratory diseases and may contribute to their pathogenesis through mechanisms involving mitochondrial dysfunction, inflammatory responses, and metabolic reprogramming. This review summarizes the molecular mechanisms of cuproptosis, key regulatory genes, and its roles in respiratory diseases, aiming to provide a theoretical basis and research direction for further exploration of cuproptosis-related mechanisms.