In a recent study published in the British Journal of Pharmacology, researchers at the University of Georgia found that the therapy triciribine could be able to reverse or stop pulmonary hypertension and pulmonary fibrosis progression.
Pulmonary fibrosis occurs when lung tissue becomes damaged and scarred. This thickened, stiff tissue makes it more difficult for the lungs to work properly. As pulmonary fibrosis worsens, patients become progressively more short of breath. According to the Coalition for Pulmonary Fibrosis, the condition affects 130,000 people in the United States.
Pulmonary hypertension is a type of high blood pressure that affects the arteries in the lungs and the right side of the heart. According to the Centers for Disease Control and Prevention, the condition is rare and affects 15 to 50 cases per million people.
“The average life expectancy for people with these diseases is only about five years after diagnosis, and while the drug treatments we currently have may help improve quality of life, they don’t reduce mortality,” said Somanath Shenoy, co-author of the paper and associate professor in UGA’s College of Pharmacy. “Our tests show that treatment with triciribine can halt disease progression and may even reverse some of the damage to lung tissue.”
The team used pulmonary hypertension and pulmonary fibrosis mouse models to assess the effect of triciribine, a drug agent that is able to inhibit the production of the Akt1 protein.
Results from previous studies showed that Akt1 is partly responsible for the development of myofibroblasts, cells that migrate to the sites of injury to aid in wound healing. When there is an unregulated production of these cells, they cause scarring, leading to loss of functional blood vessels and fibrosis in the lungs.
In the study, when mice had the disease symptoms, the researchers injected them triciribine once per day for three weeks, with results showing a slowing in the scarring and loss of lung vasculature. They even found that tissue in the mice’s lungs returned to normal.
“To our knowledge, this is the first direct evidence that Akt1 causes disease onset and progression of pulmonary fibrosis and pulmonary hypertension,” Shenoy said. “We have also tested this process in human cells taken from diseased lung tissue, and we see very similar results.”
The team then examined mice genetically modified with the Akt1 pathway absence, with results showing that these mice did not develop any symptoms of the disease. Based on the results, the researchers suggested a new direction for the cause of the disease. However, these findings are still preliminary, and more studies are needed before the researchers can examine the efficacy of triciribine in humans. A human version of triciribine could be administered orally, eliminating the need for daily injections.
“We still need to identify the downstream effects of Akt1 inhibition to see if there are any negative side effects,” Shenoy said in the news release. “But if these tests go well, we hope to begin human trials within the next three to five years.”
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