Researchers at the University of Georgia have found a potential drug treatment for two fatal lung diseases. Pulmonary fibrosis and pulmonary hypertension currently are virtually universally fatal and up until now efforts to find a way to treat them did not bring much success. However, now scientists have discovered that the drug triciribine may reverse or halt the progression of these two diseases.
Even though causes for pulmonary fibrosis and pulmonary hypertension have not been identified, these diseases affect many people every year. Pulmonary fibrosis is more common with about 48,000 new cases diagnosed annually in United States alone. It occurs when lung tissue becomes scarred and leads to loss of lung function and reduced oxygen supply to the blood. Pulmonary hypertension is rare, with only about 15 to 50 cases per million people, but is dangerous nevertheless. It involves an increase of blood pressure in the arteries of the lung that can eventually lead to heart failure. Scientists have been puzzling how to treat these diseases and now it looks like they are one step closer to a major breakthrough.
Somanath Shenoy, co-author of the research, said that the new tests in the study have “show that treatment with triciribine can halt disease progression and may even reverse some of the damage to lung tissue”. With current therapies life expectancy for people with these diseases is only about five years after diagnosis. Currently used drugs can only improve quality of life for these years, but do not reduce mortality, which makes these discoveries even more important.
Triciribine, which inhibits production of a protein called Akt1. The team of scientists have used mouse models to test this drug against pulmonary hypertension and pulmonary fibrosis. Previously conducted research has showed that Akt1 is at least partly responsible for the development of myofibroblasts, cells that migrate to the sites of injury to aid in wound healing. However, if these cells become unregulated, it can lead to scarring in lung tissue and loss of functional blood vessels in the lungs.
The course of the research is pretty much self-explanatory. Researchers caused these diseases in mice and waited until mice began to exhibit symptoms. Then injected the mice with triciribine once daily for a period of three weeks. Results were surprisingly good – characteristic scarring and loss of lung vasculature was slowed in every mouse. Furthermore, the lung tissue of some mice began to return to normal, which gives hope that disease may not only be slowed down, but even reversed.
Scientists have conducted similar tests on human cells taken from diseased lung tissue, and have noticed very similar results. It is first time it has been proved that Akt1 causes disease onset and progression of pulmonary fibrosis and pulmonary hypertension. Scientists produced genetically modified mice that do not possess the Akt1 pathway and none of them developed symptoms of these diseases, which further confirms that Akt1 plays an important role in development of pulmonary fibrosis and pulmonary hypertension.
However, these results are only preliminary and more research is needed to find if there are any side effects of the triciribine, how it will work with humans. Scientists hope to begin human trials within the next three to five years and say that human version of triciribine could be administered orally, eliminating the need for daily injections. Although, these diseases are not very common, these discoveries will still help many people who suffer from these fatal conditions.