Circular RNA circTrpc6-induced tau phosphorylation contributes to neuronal injury and cognitive decline via miR-485-5p/eIF4E axis in senescence-accelerated mouse prone 8 mice.

Chronic obstructive pulmonary disease (COPD) is a major global health concern and remains one of the leading causes of morbidity and mortality worldwide. Although cigarette smoking has traditionally been recognized as the principal risk factor for COPD development, recent studies indicate that COPD is a heterogeneous disorder with multifactorial etiologies extending beyond smoking. Contributing factors include genetic susceptibility, early-life events, such as in utero exposures, previous respiratory infections, and harmful environmental exposures [, ]. To capture this etiological heterogeneity in more detail, the Lancet Commission recently proposed a novel classification framework for COPD encompassing five distinct subtypes based on predominant risk factors: Type 1 (COPD-G, genetic), Type 2 (COPD-D, developmental), Type 3 (COPD-I, infection-related), Type 4 (COPD-C, cigarette smoking-related), and Type 5 (COPD-P, pollution- or environmental-related) []. This etiotype-based model has been integrated into the 2023 update of the Global Initiative for Chronic Obstructive Lung Disease (GOLD) report, which underscores the importance of a more individualized approach to COPD diagnosis and management [, ]. Despite the recent adoption of this etiological classification, few studies have investigated differences in clinical characteristics or treatment patterns among the various COPD subtypes. Blood eosinophil count (BEC) has emerged as a valuable biomarker for predicting responsiveness to inhaled corticosteroid (ICS) therapy [, ]; however, data on the distribution of eosinophil counts and ICS prescription practices across etiological subtypes remain limited. In particular, patients with infection-related COPD—defined by a history of respiratory infections such as tuberculosis—may exhibit distinct immunologic profiles and therapeutic responses compared to those with smoking-related COPD [–].