Key Protein Could Prevent Abnormal Arterial Changes in Pulmonary Hypertension

Key Protein Could Prevent Abnormal Arterial Changes in Pulmonary Hypertension

Researchers at the Medical College of Georgia at Augusta University found a specific protein that seems to cause abnormal blood vessel growth in pulmonary arterial hypertension (PAH). The protein, called galectin-3, or gal-3, could be a new treatment target.

Scientists are studying a drug called GR-MD-02 that could be a treatment for PAH, said Dr. David Fulton, director of the Vascular Biology Center at the Medical College of Georgia (MCG) in a press release. GR-MD-02 acts by blocking gal-3 levels, according to data presented at the 2016 American Thoracic Society Conference. Investigators will continue to develop the drug in collaboration with Atlanta-based Galectin Therapeutics.

PAH refers to high blood pressure in the lungs, in which blood vessels can be transformed into twisted arteries that prevent normal blood flow. It is a condition that worsens over time and can be fatal, since pressure in the lung arteries can strain the heart. Although PAH currently has no cure, several medications are used to control its symptoms. A gal-3 blocker could target the cause of the disease, rather than just the symptoms.

Dr. Scott Barman and Dr. David Fulton. Credit: Phil Jones
Dr. Scott Barman and Dr. David Fulton. Credit: Phil Jones

Fulton and Dr. Scott Barman, pulmonary vascular biologist in the MCG Department of Pharmacology and Toxicology, received a $2.2 million grant from the National Institutes of Health (NIH) to study gal-3 in PAH.

“Excessive constriction makes the vessels small in the first place; inflammation and remodeling make it a permanent anatomical alteration,” Barman said.

Right heart failure is the most common cause of death in people with PAH, since the right portion of the heart has to work harder to force blood through narrow arteries.

“The lung circulation is a high-capacity, low-resistance environment,” Fulton said. “Any increase in resistance to blood flow is really damaging.”

The researchers not only plan to study how to block excessive levels of gal-3 in PAH, but also to understand why increases in this protein level happen in the first place. “Where is it coming from and where is it hitting?” Barman asked. Another goal is to understand how gal-3 influences blood vessel reorganization.

The team also plans to test whether gal-3 based treatments could be effective in advanced PAH. “The more we can reverse it later in disease the more applicable the therapy becomes,” Barman said.

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