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Peer-reviewedCC BY 4.0International Journal of Molecular Sciences

Cuproptosis in Inflammation-Related Respiratory Diseases

  • Qiaoli Fu1
  • Yuanyuan Zheng1
  • Yinchun Zou1
  • Xinyi Cui2
  • Rui Wei3
  • Ying Gu1
  • Lijun Qin1
  • Shibo Sun1
  1. 1First Department of Respiratory and Critical Care Medicine, The First Affiliated Hospital of Kunming Medical University, Kunming 650032, China
  2. 2Department of Clinical Medicine, Kunming Medical University, Kunming 650500, China
  3. 3Department of Emergency Medicine, The First Affiliated Hospital of Kunming Medical University, Kunming 650032, China
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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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Cite

BibTeXRIS
BibTeX
@article{fu2026cuproptosis,
  title = {{Cuproptosis in Inflammation-Related Respiratory Diseases}},
  author = {Qiaoli Fu and Yuanyuan Zheng and Yinchun Zou and Xinyi Cui and Rui Wei and Ying Gu and Lijun Qin and Shibo Sun},
  journal = {International Journal of Molecular Sciences},
  year = {2026},
  month = oct,
  doi = {10.3390/ijms27209218},
  url = {https://www.mdpi.com/1422-0067/27/20/9218},
  note = {CC BY 4.0},
}
RIS
TY  - JOUR
TI  - Cuproptosis in Inflammation-Related Respiratory Diseases
AU  - Qiaoli Fu
AU  - Yuanyuan Zheng
AU  - Yinchun Zou
AU  - Xinyi Cui
AU  - Rui Wei
AU  - Ying Gu
AU  - Lijun Qin
AU  - Shibo Sun
PY  - 2026
DA  - 2026/10/01
JO  - International Journal of Molecular Sciences
DO  - 10.3390/ijms27209218
UR  - https://www.mdpi.com/1422-0067/27/20/9218
AB  - 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.
SN  - 1422-0067
ER  -