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- W1963543097 abstract "Nitric oxide (NO) exerts ubiquitous signaling via posttranslational modification of cysteine residues, a reaction termed S-nitrosylation. Important substrates of S-nitrosylation that influence cardiac function include receptors, enzymes, ion channels, transcription factors, and structural proteins. Cardiac ion channels subserving excitation-contraction coupling are potentially regulated by S-nitrosylation. Specificity is achieved in part by spatial colocalization of ion channels with nitric oxide synthases (NOSs), enzymatic sources of NO in biologic systems, and by coupling of NOS activity to localized calcium/second messenger concentrations. Ion channels regulate cardiac excitability and contractility in millisecond timescales, raising the possibility that NO-related species modulate heart function on a beat-to-beat basis. This review focuses on recent advances in understanding of NO regulation of the cardiac action potential and of the calcium release channel ryanodine receptor, which is crucial for the generation of force. S-Nitrosylation signaling is disrupted in pathological states in which the redox state of the cell is dysregulated, including ischemia, heart failure, and atrial fibrillation." @default.
- W1963543097 created "2016-06-24" @default.
- W1963543097 creator A5003169178 @default.
- W1963543097 creator A5047146685 @default.
- W1963543097 creator A5052092118 @default.
- W1963543097 creator A5060088000 @default.
- W1963543097 creator A5085774808 @default.
- W1963543097 date "2009-09-01" @default.
- W1963543097 modified "2023-09-23" @default.
- W1963543097 title "S-Nitrosylation of Cardiac Ion Channels" @default.
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