The latest research investigating how cellular iron metabolism is regulated in the lungs of patients with COPD and how dysregulation of iron uptake contributes to the disease process has identified the culprit — a gene they previously found to increase patients’ susceptibility to the progressive lung disease. This gene, called IRP2, is responsible for regulating iron uptake in cells. The team’s discovery was significant because it validates the results of a 2009 study that implicated IRP2 in the disease’s development and demonstrates how the gene supports COPD. The findings also illustrate that IRP2 may be a powerful therapeutic target. The research at the laboratory of Trinity’s School of Medicine and Tallaght University Hospital in Dublin, led by Dr Suzanne Cloonan, Associate Professor in Respiratory Medicine, aimed to figure out where in the lung this iron accumulates and how this excess of iron affects the development of COPD. “We are asking the following questions: Where does this iron come from given that cigarette smoke contains very little iron?

What cell types are important in iron accumulation in the lung? Does having more iron promote the growth of bad bacteria rendering COPD patients more susceptible to infection?” Dr Cloonan said in a report. The team also found out how iron is transported into and out of the mitochondrion (mitochondria are the ‘powerhouses’ of the cell). Mitoferrin-2 and mitoferrin 1 are mitochondrial membrane proteins that are thought to be involved in iron transport across the mitochondrial inner membrane into the mitochondrial matrix. The researchers investigated how these transporters contribute to normal mitochondrial function, metabolism and dynamics in the cell and how they coordinate with other aspects of cellular iron regulation as well.