Cuproptosis in Inflammation-Related Respiratory Diseases

Cuproptosis is a newly identified form of regulated cell death. The core molecular events of cuproptosis involve copper homeostasis dysregulation, aggregation of mitochondrial lipoylated proteins, loss of iron–sulfur cluster proteins, and mitochondrial proteotoxic stress. Multiple signaling pathways regulate cuproptosis, such as the mitogen-activated protein kinase (MAPK), hypoxia-inducible factor-1α (HIF-1α), and the p53 pathway. Cuproptosis plays an important role in various inflammation-related respiratory diseases, including lung cancer, acute lung injury/acute respiratory distress syndrome (ALI/ARDS), asthma, chronic obstructive pulmonary disease (COPD), and tuberculosis. Cuproptosis inhibits malignant progression and therapeutic resistance in lung cancer, while it aggravates ALI/ARDS. In addition, cuproptosis promotes airway inflammation and remodeling of asthma. However, the role of cuproptosis in COPD and tuberculosis remains unclear. Moreover, the mechanism of cuproptosis affecting inflammation-related respiratory diseases is unclear. Accordingly, cuproptosis may play an important role in various inflammation-related respiratory diseases.