Scientists discover new target in the treatment of pulmonary hypertension

Download PDF Copy

May 1, 2018

In a recent study, scientists found that eliminating the FoxM1 gene could improve outcomes for patients with pulmonary hypertension.

Credit: Leigh Prather/Shutterstock.com

The study was conducted by scientists at Stanley Manne Children's Research Institute at Ann & Robert H. Lurie Children's Hospital of Chicago, and was recently published in the American Journal of Respiratory and Critical Care Medicine.

Pulmonary hypertension is an acute lung disease that affects the right side of the heart. Sadly, the five-year survival rate is just 50 percent.

The FoxM1 gene influences cell growth and plays a role in the proliferation of cancer cells. Currently, research into FoxM1 gene is still in the preclinical stage but it is hoped that the discovery will help stimulate the production of novel drugs to reverse the effects of vascular remodeling.

This is a major process associated with pulmonary hypertension wherein the artery walls of the lungs begin to thicken, causing breathlessness.

Our study shows that when we deleted the FoxM1 gene in the smooth muscle cells of the artery in mice, the result was thinner artery walls, reduced blood pressure in the lung and improved right heart function. We can use a compound against FoxM1 to reverse vascular remodeling in rat models of the disease. "
Dr. Zhiyu Dai, The Manne Research Institute

The team found that in pulmonary hypertension, damaged endothelial cells found on the arteries inner wall discharge multiple growth factors, which activate the FoxM1 gene. The researchers think that this may initiate a series of signaling pathways leading to pulmonary hypertension.

The researchers will now begin exploring FoxM1 inhibitors and their potential in the treatment of pulmonary hypertension.

We will now focus on developing new drugs that will inhibit the FoxM1 gene and hopefully improve outcomes for patients with pulmonary hypertension"
Dr. Zhiyu Dai, The Manne Research Institute

Source:

https://www.eurekalert.org/pub_releases/2018-04/arh-sin043018.php