Therapeutic approach to COPD by targeting pulmonary associated cell signaling pathways

Chronic Obstructive Pulmonary Disease (COPD) is a respiratory disorder distinguished by airway inflammation, oxidative stress, and impaired lung regeneration. The aim of this review is to explore the mechanistic involvement of key signaling pathways in COPD progression, focusing on their impact on inflammation, oxidative stress, airway remodeling, and fibrosis. We further highlight the potential of pathway-targeted therapies in COPD and the need for further research to develop novel interventions that enhance lung repair and reduce disease progression. Several key signaling pathways, including Hedgehog (Hh), Wnt, Mitogen-Activated Protein Kinase (MAPK), Nuclear Factor Erythroid 2-Related Factor 2 (Nrf2), Bone Morphogenetic Protein (BMP), and SMAD, play crucial roles in the disease development of COPD and pulmonary fibrosis. The review highlights the role of key signaling molecules in glucocorticoid insensitivity in COPD along with the protective role of Prostaglandin E2 in reducing airway inflammation. This has important implications in terms of Cyclooxygenase inhibitor use in asthma and COPD. Understanding these molecular mechanisms can pave the way for precision medicine approaches in COPD management.