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Redox Regulation of Ion Channels and Receptors in Pulmonary Hypertension
Author(s) -
Laura Weise-Cross,
Thomas C. Resta,
Nikki L. Jernigan
Publication year - 2019
Publication title -
antioxidants and redox signaling
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.277
H-Index - 190
eISSN - 1557-7716
pISSN - 1523-0864
DOI - 10.1089/ars.2018.7699
Subject(s) - oxidative stress , hypoxic pulmonary vasoconstriction , reactive oxygen species , microbiology and biotechnology , receptor , intracellular , mitochondrion , ion channel , redox , context (archaeology) , homeostasis , vasoconstriction , pulmonary hypertension , chemistry , biochemistry , biology , medicine , endocrinology , paleontology , organic chemistry
Significance: Pulmonary hypertension (PH) is characterized by elevated vascular resistance due to vasoconstriction and remodeling of the normally low-pressure pulmonary vasculature. Redox stress contributes to the pathophysiology of this disease by altering the regulation and activity of membrane receptors, K + channels, and intracellular Ca 2+ homeostasis. Recent Advances: Antioxidant therapies have had limited success in treating PH, leading to a growing appreciation that reductive stress, in addition to oxidative stress, plays a role in metabolic and cell signaling dysfunction in pulmonary vascular cells. Reactive oxygen species generation from mitochondria and NADPH oxidases has substantial effects on K + conductance and membrane potential, and both receptor-operated and store-operated Ca 2+ entry. Critical Issues: Some specific redox changes resulting from oxidation, S-nitrosylation, and S-glutathionylation are known to modulate membrane receptor and ion channel activity in PH. However, many sites of regulation that have been elucidated in nonpulmonary cell types have not been tested in the pulmonary vasculature, and context-specific molecular mechanisms are lacking. Future Directions: Here, we review what is known about redox regulation of membrane receptors and ion channels in PH. Further investigation of the mechanisms involved is needed to better understand the etiology of PH and develop better targeted treatment strategies.

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