According to an enlightening article published in Cell it seems possible that the damage caused to lungs by smoking be reversed with the help of a new method. In the context that chronic obstructive pulmonary disease is the third highest killer disease in the USA, this is a very significant finding.
Norbest Weissman, a scientist from University of Giessen Lung Center in Germany, pointed that there was no clarity on what causes the disease and hence, no effective therapy could be worked out to reverse or stop lung destruction in emphysema. In 20 years of research, there had been no path-breaking news until now.
For a long time it was known that COPD would also mean high blood pressure in the lungs, though it was not clear whether this was a cause or trigger. The research that Norbest Weissman and his colleagues uncovered evidence that high blood pressure caused by changes in the pulmonary blood vessels set the scene for the development of emphysema. The study isolated and enzyme – iNOS or nitric oxide synthase – that induces these changes by catalyzing the formation of nitric oxide.
In other words, iNOS increases the formation nitric oxide (NO), which in normal quantity is essential for maintaining vascular health by opening up blood vessels. When in excess, however nitric oxide causes mutation of the molecule (through chemical reaction) to form peroxynitrite, which destroys lung tissue. As Weissman said, “Simply put, peroxynitrite can modify protein functions, leading to the destruction of lung tissue.”
The finding and understanding of the role of this enzyme – iNOS – can prove immensely beneficial to human beings fighting diseases that have caused advanced lung destruction. Research showed that blocking the iNOS and/ or iNOS activity in mice protected them from COPD and changes to their lung blood vessels. Over time, it reversed the course of the disease.
The good news here is that the iNOS inhibitor showed no side effects in clinical trials. Weissman said that there is hope for this drug to be used in inhalation therapies to reverse damage caused to lungs by COPD.