Apelin は Elastase 誘導性肺気腫モデルマウスにおいて肺炎症を抑制し COPD 病態を改善する

<p>Chronic obstructive pulmonary disease (COPD) is a refractory respiratory disorder characterized by airway inflammation, emphysema, and mucus retention, primarily classified into two subtypes (airway- and emphysema-dominant type). In recent years, COPD has been recognized not only as a pulmonary disease but also as a systemic inflammatory condition, demanding a comprehensive therapeutic approach with various targets. Recently, the bioactive peptide apelin has gained attention as a therapeutic target for COPD-associated comorbidities. Interestingly, the expression of apelin and its receptor was found to be significantly decreased in various COPD animal models, but the exact impact of apelin on COPD pathogenesis remains unclear. In this study, intraperitoneal administration of apelin did not have any significant impact on COPD pathogenesis in airway epithelial-specific Na⁺ channel (ENaC) overexpressing mice (airway-dominant type), which was established in our laboratory. In contrast, intraperitoneal administration of apelin to the elastase model (emphysema-dominant type) significantly reduced the total cell and neutrophil counts in bronchoalveolar lavage fluid (BALF). Additionally, it significantly improved emphysema and suggested that apelin could ameliorate the inflammatory state in emphysema-dominant COPD pathogenesis. This study is the first to reveal the potential of apelin in improving emphysema-dominant COPD pathogenesis, proposing apelin as a novel therapeutic target for this particular subtype of COPD.</p>