ANN ARBOR, Mich. A diagnosis of Idiopathic Pulmonary Fibrosis is not much better than a death sentence: there is no treatment and the survival rate is less than three years.
But researchers at the University of Michigan have discovered 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. The researchers' findings will be published in the September issue of the journal Nature Medicine.
"We've identified the target. We know the enemy now," said Subramaniam Pennathur, M.D., assistant professor of internal medicine/nephrology. "This is the first study that shows pulmonary fibrosis is driven by this NOX4 enzyme.
"But what's really significant is this discovery may have relevance to fibrosis in other organ systems, not just the lung."
So those suffering from common cardiac or kidney diseases, which often involve fibrosis, also may benefit from treatments stemming from this research, Pennathur said.
Pennathur said continued support from the National Institutes of Health will eventually allow researchers to take the treatment to human studies. The University of Michigan also has filed for patent protection and is currently looking for a licensing partner to help bring the technology to market.
The discovery was made in the University of Michigan lab of Victor J. Thannickal, M.D. He was assisted by Louise Hecker, Ph.D., a post-doctoral research fellow.
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
|Contact: Mary Masson|
University of Michigan Health System