Although COPD is a leading cause of morbidity and mortality worldwide, there is currently no cure for the disease. Providing patients with concentrated oxygen therapy and instruction on breathing techniques increases survival rates.
In a new study published in Disease Models & Mechanisms (DMM), dmm.biologists.org, collaborative findings by European researchers demonstrate that an antioxidant protein, sestrin, triggers molecular pathways that induce some of the critical lung changes associated with COPD. By genetically inactivating this protein, they were able to improve the elastic features of the lung in a mouse model of emphysema. These authors believe that by inhibiting the antioxidant sestrin protein, they prevent the accelerated degradation of elastic fibres within the lung. This suggests that patients with COPD could benefit from treatment with drugs that block sestrin function.
Although sestrin is an antioxidant protein, the authors found that this characteristic of the protein is not likely to influence its effects on COPD progression in the lung. The negative effects of sestrin on lung elasticity results from its suppression of genes whose products maintain elastin. Elastin makes the lung flexible so that it can expand and contract. Without elastin fibres, the lung becomes rigid and increasingly unable to provide for gas exchange.