Abstract
Potassium channels play diverse roles in regulating the behavior of pulmonary artery smooth muscle cells. In 2013, the discovery of KCNK3 (TASK1) as a new predisposing gene for pulmonary arterial hypertension (PAH) led to an update in the Nice Classification regarding the genetic origin of PAH. Decreased current via KCNA5 (Kv1.5) plays a key role in determining pulmonary arterial tone and vascular remodeling. The transformation of smooth muscle cells causes ion channel switching, such as the loss of BKca (Kca1.1) and the gain of IKca (Kca3.1), in immature proliferative smooth muscle cells and also induces cell migration, proliferation, and apoptosis resistance. Pulmonary smooth muscle cells from PAH patients demonstrate many cellular abnormalities linked to potassium channels. This review summarizes the current knowledge regarding the involvement of potassium channels in the development of PAH and discusses potential treatments to be developed in the near feature.
