【Purpose】
COPD is a refractory pulmonary disease characterized by bronchitis, emphysema and mucus stasis. Because COPD is a multifactorial disease and represents various symptoms for each patient, previous studies which regard COPD as a single disease have limits. Therefore, to establish personalized medicine for COPD we need research developments based on phenotype or endotype classification. Here, I focused on T₃ which has long been known to act as an essential factor for development and growth in the lung. This study aims to elucidate the pathophysiological role of T₃ using COPD mouse model simulating disease type classification (emphysema- or airway-dominant). 
【Methods & results】
In this study, I chose elastase-induced model and C57BL/6-βENaC-Tg mice as mouse models of emphysema- and airway-dominant COPD, respectively. I intratracheally administered T₃ (40 or 80 μg/kg, every other day) to elastase-induced mice for 21 days or C57BL/6-βENaC-Tg mice for 12 days. In elastase-induced model, T₃ treatment improved emphysema and, partially, the respiratory function with upregulation of the expression of Ppargc1a (the master regulator of mitochondrial biogenesis) and Gclm (an oxidative stress-related factor) after one T₃ injection. On the other hand, in C57BL/6-βENaC-Tg mice T₃ treatment did not improve COPD pathology.
【Discussion】
These results emphasize the importance of research developments based on phenotype or endotype classification considering that T₃ effect is different between two COPD models.