Pulmonary arterial hypertension (PAH) is a serious life threatening disease that leads to
right heart failure and death. Elevated pulmonary vascular resistance (PVR) is the main pathophysiological
component that leads to elevated pulmonary arterial pressures and increased right ventricular
afterload. Increased PVR is related to different mechanisms that include vasoconstriction, proliferative
and obstructive remodeling of the pulmonary vessel wall and in situ thrombosis. Numerous molecular,
genetic and humoral abnormalities have been proposed to play an important role in pulmonary vasoconstriction and remodeling.
Of those, calcium (Ca+2) is a well recognized parameter involved in the pathogenetic mechanisms of PAH, because
of its twofold role in both vasoconstriction and pulmonary artery smooth muscle cell (PASMC) proliferation. The
aim of this review is to focus on Ca+2 handling and dysregulation in PASMC of PAH patients.
Keywords: Calcium handling, pulmonary arterial hypertension, vascular proliferation, vasoconstriction, calcium signaling,
intracellular calcium handling, intercellular calcium handling.
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