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Cuproptosis in Inflammation-Related Respiratory Diseases
Qiaoli Fu1, Yuanyuan Zheng1, Yinchun Zou1
1First Department of Respiratory and Critical Care Medicine, The First Affiliated Hospital of Kunming Medical University, Kunming 650032, China.
Abstract:
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.
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