They found that targeting of a novel gene utilizing genetic and pharmacologic strategies was successful in treating pulmonary fibrosis in mice and will be developed for future testing in humans.
The treatments attack an oxidant-generating enzyme, NOX4, that researchers discovered is involved in the fibrotic process - which involves scar-like tissue formation in an organ such as the lung.
"We've identified the target. We know the enemy now. This is the first study that shows pulmonary fibrosis is driven by this NOX4 enzyme," said Subramaniam Pennathur, M.D., assistant professor of internal medicine/nephrology.
"But what's really significant is this discovery may have relevance to fibrosis in other organ systems, not just the lung," Pennathur added.
Pennathur said that those suffering from common cardiac or kidney diseases, which often involve fibrosis, also may benefit from treatments stemming from this research.
The discovery was made in the University of Michigan lab of Victor J. Thannickal, M.D.
Thannickal said the study points to a very viable treatment strategy for idiopathic pulmonary fibrosis, and researchers saw success both in mouse models of lung fibrosis and in fibrogenic cells isolated from lungs of patients with Idiopathic Pulmonary Fibrosis.
"It remains to be seen if fibrosis is reversible. But therapeutic targeting of this pathway this may allow us to halt the progression of fibrosis and preserve lung function," he said.
The findings will be published in the September issue of the journal Nature Medicine.