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“Toxic” Estrogen By-Product Linked With Pulmonary Arterial Hypertension
In a study funded by the British Heart Foundation and published in Circulation, scientists at the University of Glasgow showed that high levels of an enzyme in the lungs called CYP1B1—which breaks down estrogen into harmful smaller molecules—could play a role in the development of pulmonary arterial hypertension (PAH).
PAH often affects younger, premenopausal women. The symptoms of the disease include breathlessness and chest pain. The symptoms worsen as lung blood pressure increases, and the disorder is often fatal. More than one in ten patients die within the first year after diagnosis. Although treatments are available, they are often not effective.
The new study shows a link between high levels of a harmful molecule produced from the breakdown of estrogen by CYP1B1 and the development of PAH. The findings could help lead to new treatments for the disease.
The researchers showed that CYP1B1 levels were elevated in the lungs of mice with PAH, and that lowering CYP1B1 levels reduced the severity of the disease. A “toxic” by-product of estrogen, called 16a-hydroxyestrone, was found in elevated amounts in the urine of mice that developed the condition.
Importantly, the researchers also examined a small number of lung samples from human patients with pulmonary hypertension, all of whom had elevated levels of CYP1B1. This finding suggests that targeting the enzyme with a specific drug in the future might make a difference for patients.
For more information, visit the University of Glasgow Web site.