S-Nitrosylation in Cardiovascular Disorders: The State of the Art

Figures

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  Figure 1. Formation pathway of S-nitrosothiol in mammals. (1) Direct addition catalyzed by transition metal; (2) Autoxidation of NO; (3) Free radical recombination; (4) Transnitrosation. “M” indicates a metal or other cation. Transition metals, such as copper (II) or iron (III), act as electron acceptors. Divalent cations, like zinc, act as catalysts.

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  Figure 2. Mechanism of protein S-nitrosylation in systemic hypertension. ACTA2: actin alpha 2, AngII: angiotensin II, AT1R: angiotensin type 1 receptor, CaMKIIγ: calcium/calmodulin-dependent protein kinase II γ, CaM: calmodulin, DAG: diacylglycerol, GTP: guanosine triphosphate, IP3: inositol triphosphate, JAK: Janus kinase, MLCK: myosin light-chain kinase, NO: nitric oxide, PCNA: proliferating cell nuclear antigen, PE: phenylephrine, PIP2: phosphatidylinositol 4, 5-diphosphate, PKC: protein kinase C, PLC: phospholipase C, RhoA: Ras homolog gene family member A, ROCK: Rho-associated kinase, SNO: S-nitrosylation, STAT3: signal transducer and activator of transcription 3, VEGF-A: vascular endothelial growth factor-A, VEGFR2: vascular endothelial growth factor receptor 2, α1-AR: α1-adrenergic receptor.

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  Figure 3. Mechanism of protein S-nitrosylation in pulmonary arterial hypertension (PAH). CaM: calmodulin, Caspase3: cysteine proteinase 3, DAG: diacylglycerol, IP3: inositol triphosphate, LLO: listeriolysin-O, LPS: lipopolysaccharide, MLCK: myosin light-chain kinase, MT: metallothionein, NO: nitric oxide, PE: phenylephrine, PIP2: phosphatidylinositol 4, 5-diphosphate, PKC: protein kinase C, PLC: phospholipase C, RhoA: Ras homolog gene family member A, ROCK: Rho-associated kinase, SNO: S-nitrosylation, TLR4: Toll-like receptor 4, VE-cadherin: vascular endothelial-cadherin, α1-AR: α1-adrenergic receptor.

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  Figure 4. Mechanism of protein S-nitrosylation in heart failure. ANT1: adenine nucleotide translocase 1, CDK2: cyclin-dependent kinase 2, eIF2Bε: eukaryotic initiation factor 2B epsilon subunit, GSK-3β: glycogen synthase kinase-3β, HDAC1: histone deacetylase 1, HSP90: heat shock protein 90, IKKα, β, γ: IκB kinase α, β, γ, iNOS: inducible nitric oxide synthase, IL-1β: interleukin-1β, iNOS: inducible nitric oxide synthase, IRE1α: inositol-requiring enzyme 1α, MLP: muscle LIM protein, NF-κB: nuclear factor-kappa B, NLRP3: nod-like receptor protein 3, NO: nitric oxide, pRb: retinoblastoma protein; RIP3: receptor-interacting protein 3, SNO: S-nitrosylation, TLR4: Toll-like receptor 4, Xbp1s: X-box-binding protein 1.

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  Figure 5. Mechanism of protein S-nitrosylation on myocardial infarction. Akt: protein kinase B, ANT1: adenine nucleotide translocase 1, AP-1: activator protein-1, ASK-1: apoptosis signal-regulating kinase 1, CypD: cyclophilin D, DHETs: dihydroxyeicosatrienoic acids, EETs: epoxyeicosatrienoic acids, eNOS: endothelial nitric oxide synthase, GRK2: G protein-coupled receptor kinase 2, HSP90: heat shock protein 90, iNOS: inducible nitric oxide synthase, IRI: ischemia–reperfusion injury, JNK: c-Jun NH2-terminal kinase, mPTP: mitochondrial permeability transition pore, NO: nitric oxide, PAF: platelet-activating factor, p38MAPK: p38 mitogen-activated protein kinase, ROS: reactive oxygen species, sEH: soluble epoxide hydrolase, SMAD3: SMAD family member 3, SNO: S-nitrosylation, TGF-β: transforming growth factor-β, Trx: thioredoxin, VDAC: voltage-dependent anion-selective channel.

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  Figure 6. Mechanism of protein S-nitrosylation on arrhythmia. AngII: angiotensin II, AT1R: angiotensin type 1 receptor, Cav1, 3: Caveolin 1, 3, CO: carbon monoxide, Cx43: connexin 43, eNOS: endothelial nitric oxide synthase, NO: nitric oxide, ROS: reactive oxygen species, RyR2: ryanodine receptor 2, SERCA2: sarcoplasmic/endoplasmic reticulum calcium ATPase 2, SNO: S-nitrosylation, nNOS: neuronal nitric oxide synthase.