Chronic obstructive pulmonary disease (COPD) is a prevalent and deadly lung disease (third leading cause of death worldwide), caused mainly by tobacco smoke and air pollutants. With approximately 300 million patients worldwide, the economic burden is projected to reach INT$ 4.326 trillion by 2050. The key problem underlying COPD pathogenesis is increased tissue destruction and abnormal tissue repair, leading to irreversible airflow obstruction and lung function decline. Current treatments alleviate symptoms, but do not address the disease. There is a major unmet need for regenerative (pharmacological) therapeutics targeting COPD’s root cause.
Our research focuses on specific lung cells that are essential for keeping our lungs healthy. These cells, called type 2 alveolar epithelial cells (AT2), need signals from other lung cells, called fibroblasts, to work properly. Using advanced techniques, we discovered a protein called osteoglycin (OGN) that the fibroblasts release. In tests mimicking COPD in the lab, we found that OGN helps the lungs regenerate better than other proteins released by fibroblasts. This finding suggests a new approach to treating COPD by helping the lungs repair themselves, rather than just treating symptoms. If successful, this new therapy could completely change how we manage COPD, potentially offering better outcomes for patients.
Chronic obstructive pulmonary disease (COPD) is a prevalent and deadly lung disease (third leading cause of death worldwide), caused mainly by tobacco smoke and air pollutants. With approximately 300 million patients worldwide, the economic burden is projected to reach INT$ 4.326 trillion by 2050. The key problem in COPD pathogenesis is excessive tissue destruction combined with abnormal tissue repair, leading to irreversible airflow obstruction and progressive lung function decline. Current treatments alleviate symptoms but do not address the root cause of the disease, underscoring the urgent need for regenerative (pharmacological) therapies.
Our research focuses on specific lung cells that are essential for keeping our lungs healthy. These cells, called type 2 alveolar epithelial cells (AT2), rely on signals from other neighbouring lung cells, called fibroblasts, to function properly. Using advanced techniques, we discovered a protein called osteoglycin (OGN), secreted by fibroblasts, as a key factor in this process. In laboratory models mimicking COPD, we found that OGN significantly improves lung regeneration compared to other proteins released by fibroblasts. This discovery suggests a promising new therapeutic approach for COPD, aiming to repair lung tissue rather than just managing symptoms. If successful, this new therapy could completely change how we manage COPD, potentially offering better outcomes for patients.
