Pulmonary hypertension is an unremitting disease caused by a progressive increase in blood pressure in the blood vessels of the lung; it leads to heart failure and ultimately death. Currently there are limited treatment options. However, You-Yang Zhao and colleagues, at the University of Illinois College of Medicine, Chicago, have identified in mice a new molecular pathway underlying pulmonary hypertension that they hope might provide novel therapeutic targets.
In the study, mice lacking either caveolin 1, eNOS, or both proteins were used to determine that chronic eNOS activation, secondary to loss of caveolin-1, can lead to pulmonary hypertension. Further analysis revealed that the chronic eNOS activation that induced pulmonary hypertension was associated with impaired activity of the protein PKG because it was modified by a process known as nitration.
As lung tissue from patients with a form of pulmonary hypertension known as idiopathic pulmonary arterial hypertension exhibited evidence of increased eNOS activation and PKG nitration and reduced caveolin-1 expression, the authors suggest that preventing and/or reversing PKG nitration might be of benefit to individuals with idiopathic pulmonary arterial hypertension.
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