A new and early target for treating pulmonary hypertension appears to be an enzyme that's normally key to energy production but destructive in the face of this high blood pressure inside your lungs.

It's called PFKFB3, an enzyme that helps us use glucose as an energy source. But when smoking, air pollution, congenital heart defects, and other factors start driving pressure inside the lungs up and oxygen levels down, called hypoxia, PFKFB3 levels soar and so does the damage that narrows the passageway inside the blood vessels in our lungs.

"Hypoxia is a major cause of a lot of pulmonary diseases," says Dr. Yunchao Su. In the short term, hypoxia constricts the pulmonary muscles that enable us to inhale and exhale, Su says. In the long term, it thickens the blood vessel wall, narrowing the passage for blood. In the early term, it also increases levels of PFKFB3, particularly in the pulmonary artery that takes oxygen-poor blood from the body back to the lungs for an oxygen refill.

Instead hypoxia increases PFKFB3, possibly to increase energy levels for the work at hand, but instead, it contributes to a state that leaves patients short of breath, dizzy, with swollen legs and abdomens, a racing pulse and potentially deadly heart failure.

Instead of making more blood vessels, components like the endothelial cells that line the vessels and smooth muscle cells that give vessel walls strength, thicken existing blood vessel walls and narrow the lumen through which blood flows, further raising the pressure inside the blood vessels, and reducing the blood volume they carry.

They have also seen that when they cut PFKFB3 levels essentially in half, it appears to protect mice from pulmonary hypertension, including significantly decreasing harmful inflammation and proliferation of the blood vessels in the lungs.

It also reduces levels of platelet-derived growth factor, which regulates cell growth and division, and vascular endothelial growth factor, which should have helped make more blood vessels. It even helps smooth muscle and endothelial cells resume their natural ability to die when something is amiss with them.

All this downstream curtailment that results from reducing PFKFB3 levels is why the scientists are theorizing that the enzyme has an early and key role in pulmonary hypertension, a status that makes the enzyme a logical treatment target, they say.

Current treatments for pulmonary hypertension include many of the same used for heart conditions such as digoxin to help the heart pump, diuretics to reduce fluid volume and oxygen along with drugs to help keep blood vessels from narrowing and help produce more vasodilators, according to the Pulmonary Hypertension Association. Lung or heart-lung transplants are another options when other treatments fail.

The condition often occurs in concert with others and can start with other types of heart or lung disease, according to the Centers for Disease Control and Prevention. Sometimes there is no clear cause. It can occur at any age, including in newborns, although risk increases with age. It's more common in women and blacks.

Most cells in our body use an efficient process called cell respiration, in which oxygen is used to generate ATP, the body's primary energy fuel. Also efficiently, mitochondria, powerhouses in the body, both use and make ATP. But vascular cells – and tumors alike – instead take the less efficient route of using glucose to make energy. Much of the research on PFKFB3 has been in cancer.