Serum endostatin is a novel marker for COPD associated to lung function decline and exacerbation

Backgrounds and Aims: It is well-known that angiogenesis contributes to the progression of chronic obstructive pulmonary disease (COPD) by initiating the remodeling of bronchial vasculature. However, the molecular mechanisms are incompletely understood. Endostatin, which is a member of endogenous antiangiogenic proteins activated by proteolytic cleavage, has been found to play an important role in angiogenesis and many inflammatory diseases. This research is to firstly explore whether endostatin is a biomarker in COPD. Methods: 100 stable COPD patients, 130 patients with acute exacerbation（AECOPD) and 68 healthy volunteers were recruited in this research. Lung function test was done on the healthy and stable COPD group. Serum endostatin, C-reactive protein (CRP) and vascular endothelial growth factor (VEGF) of all subjects were measured by Human Magnetic Luminex Screening Assay. Results: Serum endostatin significantly increased in stable COPD patients(89.29±30.33ng/mL) compared with healthy control (68.86±29.17ng/mL) and increased more in AECOPD patients (102.09±36.59ng/mL) (P＜0.001). Besides, stable COPD patients with frequent exacerbation (≥2 exacerbations per year) in the last one year had higher concentration of endostatin in the circulation compared to the patients with less exacerbation (P=0.037). Furthermore, endostatin was negatively correlated with FEV1/FVC (P=0.031) and FEV1% (Rho=-0.260, P=0.009) in the stable COPD group and positively related to VEGF in all the subjects (p=0.002). Conclusions: These results suggest that endostatin is a biomarker of COPD and associated with lung function decline and exacerbation. Endostatin potentially contributes to the pathogenesis of COPD.