Chronic obstructive pulmonary disease (COPD) is a chronic respiratory disease with one of the leading causes of global morbidity and mortality. Its core pathological features include irreversible airflow limitation, chronic airway inflammation, and lung tissue remodeling. In recent years, the key roles of the Wnt signaling pathway and non-coding RNAs (ncRNAs) in the pathogenesis of COPD have gained increasing attention. As a pivotal signaling cascade governing cell proliferation, differentiation and tissue repair, the Wnt pathway undergoes aberrant activation or suppression in COPD, linking closely to airway inflammation, alveolar epithelial damage and pulmonary fibrosis. Non-coding RNAs including miRNAs, lncRNAs and circRNAs modulate COPD pathogenesis via targeting core molecules of the Wnt pathway. This review summarizes the basic components and functions of the Wnt pathway and the classification and biological roles of ncRNAs and discusses their interactive mechanisms and therapeutic strategies in COPD. In addition, this review discusses the current controversies and future directions. Studies indicate that the synergistic regulatory network between the Wnt pathway and ncRNAs provides new molecular targets for the early diagnosis, prognosis assessment, and targeted therapy of COPD, highlighting potential avenues for future therapeutic development.

Considerable heterogeneity exists in patients experiencing acute exacerbation of chronic obstructive pulmonary disease (AECOPD) concerning etiology, clinical manifestations, phenotypic features, comorbidities, and treatment responsiveness. The concept of "treatable traits" is adapted to evaluate the clinical features of patients with chronic airway diseases from multiple dimensions and ultimately guiding precision treatment strategies. This prospective randomized controlled study mainly aims to evaluate the impact of accurate identification and intervention strategies guided by "treatable traits" on the prognosis of AECOPD patients.

Chronic obstructive pulmonary disease (COPD) is a long-term respiratory condition with high rates of morbidity and mortality. Its pathophysiology is complex, and currently, there are no effective clinical treatments that can fully reverse or halt the disease's progression. Animal models play a significant role in elucidating the pathogenesis of COPD, dynamic pathological processes, and evaluating potential therapeutic strategies, serving as a key to advancing in-depth research on this disease. However, existing modeling methods still face many limitations in accurately simulating the clinical symptoms, pathophysiological features, and progression of human disease, and there is a lack of standardized guidelines and industry consensus. This paper systematically reviews methods for constructing COPD animal models reported in the literature by reviewing 5,071 relevant articles from CNKI, PubMed, and Wanfang Database published in the past decade. The main models include cigarette smoke exposure, protease-induced, genetically modified, harmful substance exposure, and various combined factor models. A comprehensive review and comparison of their construction principles, procedures, pathological features, advantages, and limitations are provided. This review aims to serve as a valuable reference for COPD researchers and clinicians in the construction of animal models of COPD.