Endothelial progenitor cells and chronic obstructive pulmonary disease: From basic research to clinical application.
10.11817/j.issn.1672-7347.2024.240412
- Author:
Xue HE
1
,
2
;
Huihui ZENG
3
;
Yan CHEN
3
,
4
Author Information
1. Department of Thoracic Surgery, Second Xiangya Hospital, Central South University, Changsha
2. hexuehuxi@csu.edu.cn.
3. Research Unit of Respiratory Disease, Central South University, Changsha
4. chenyan99727@csu.edu.cn.
- Publication Type:Review
- Keywords:
chemokines;
chronic obstructive pulmonary disease;
cigarette;
endothelial progenitor cells;
smoking;
vascular endothelial growth factor
- MeSH:
Humans;
Pulmonary Disease, Chronic Obstructive/pathology*;
Endothelial Progenitor Cells/cytology*;
Animals;
Signal Transduction;
Vascular Endothelial Growth Factor A/metabolism*
- From:
Journal of Central South University(Medical Sciences)
2024;49(12):1966-1972
- CountryChina
- Language:English
-
Abstract:
Chronic obstructive pulmonary disease (COPD) is a chronic lung disease characterized by persistent airflow limitation, with vascular endothelial dysfunction being one of its key pathogenic mechanisms. Endothelial progenitor cells (EPCs), a class of progenitor cells capable of vascular repair and regeneration, play a crucial role in the pathogenesis of COPD. In COPD patients, the number and function of circulating EPCs are significantly reduced, which is closely associated with disease severity, lung function decline, acute exacerbations, nutritional status, and comorbidities. Environmental factors such as smoking, nicotine, electronic cigarettes, and particulate matter 2.5 (PM2.5) can markedly impair both the function and quantity of EPCs. The underlying mechanisms may involve the regulation of vascular endothelial growth factor/vascular endothelial growth factor receptor (VEGF/VEGFR), C-X-C motif chemokine ligand 12/C-X-C motif chemokine receptor 4 (CXCL12/CXCR4) signaling pathways, and various cytokine regulations. Moreover, animal studies have shown that intratracheal transplantation of EPCs can significantly improve lung function and pathological changes in emphysema models, suggesting that targeting EPCs may be a promising therapeutic strategy for COPD. Elucidating the molecular mechanisms of EPC mobilization, homing, and dysfunction, and evaluating the efficacy and safety of their clinical application, may offer new insights into the treatment of COPD and other chronic lung diseases.
