Description
Title: Potassium Channels in Pulmonary Arterial Hypertension: Therapeutic Targets
Abstract: The deadly disease pulmonary arterial hypertension (PAH) has a high rate of morbidity and mortality. Unfavorable remodeling in the pulmonary arterial system causes right heart failure, irreversible arterial constriction, elevated pulmonary arterial pressures, and ultimately death. The complexity of the disease pathogenesis, which is known to involve several signaling molecules (e.g., endothelin-1, prostacyclins), which are in fact targets of PAH therapy, contributes to the challenge of treating PAH. Potassium channelopathies have emerged as brand-new causes of PAH over the past ten years. More specifically, the first two potassium channelopathies in human cohorts with pulmonary arterial hypertension were identified as loss-of-function mutations in the KCNK3 gene, which encodes the two-pore-domain potassium channel KCNK3 (or TASK-1), and in the ABCC8 gene, which encodes a crucial subunit, SUR1, of the ATP-sensitive potassium channel (KATP). Furthermore, genetic changes associated with PAH have been found in the voltage-gated potassium channel (Kv) family, a third family of potassium channels. This review focuses on KCNK3, KATP, and Kv potassium channels as promising therapeutic targets in PAH, with recent experimental pharmacologic discoveries significantly advancing the field. Other ion channel genes have since been reported to be associated with PAH.
Keywords: pulmonary hypertension; ion channel; channelopathy; KCNK3; ABCC8; pharmacology
Paper Quality: SCOPUS / Web of Science Level Research Paper
Subject: Biomolecules
Writer Experience: 20+ Years
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