Smoking is a known risk factor for both chronic obstructive pulmonary disease (COPD) and idiopathic pulmonary fibrosis (IPF), but now scientists have discovered the two chronic lung diseases also share a network of genes.
The discovery should inform both future research and drug development, researchers say.
“We were able to identify a relatively large number of genes that behaved similarly in both diseases,” says Naftali Kaminski, chief of the Pulmonary, Critical Care, and Sleep Medicine section at Yale University and author of the study published in the American Journal of Respiratory and Critical Care Medicine. “This finding may suggest that there are potential core mechanisms shared by IPF and emphysema, allowing for the development of interventions to target both diseases.”
The research was a collaborative effort of scientists at Yale, Boston University, University of Colorado-Denver, Harvard, University of Pittsburgh, University of Michigan, and the Mayo Clinic. It represents the first large-scale transcriptomic study that directly compares chronic lung diseases.
“The study of COPD, IPF, or even lung cancer has been siloed for too long,” says Kaminski. “We may learn a lot by comparing and contrasting these devastating conditions.”
COPD is characterized by insufficient repair resulting in destruction of the lung tissue, while IPF is characterized by too much repair leading to excessive scarring of the lung. Both diseases cause significant morbidity and mortality rates.
The shared network of genes they uncovered is known as the p53/hypoxia pathway.
“This may suggest that the network underlies the response to the environmental causes of IPF and COPD,” says Avrum Spiro, co-corresponding author and a key collaborator on the project. “It may also be relevant to lung cancer, a condition that is more common in patients with IPF or COPD.”
The study was part of the Lung Genomics Research Consortium, funded by a National Heart, Lung, and Blood Institute grant.
Source: Yale University