Table 2.
Aberrant S-nitrosylation in Cardiovascular Disease
| SNO-protein | Disease State |
|---|---|
| Serum albumin | Pre-eclampsia107, 108 Ischemic coronary syndromes106 |
| Hemoglobin | Congestive heart failure165 Pulmonary arterial hypertension127 Sickle cell disease128 Diabetes (Type 1) 129, 130 Septic shock19 |
| Hif-1α | Pulmonary arterial hypertension60 |
| Matrix metalloproteinase 9 | Stroke166 |
| Ryanodine receptor 2 | Arrhythmogenesis, Heart failure 141 |
| L-type Ca2+ channel (α1C subunit) | Atrial fibrillation/arrhythmia135, 143, 167 |
| Cardiac Na+ channel SNC5a | Long Q/T syndrome157 |
| Slowly activating delayed-rectifier K+ channel | Atrial fibrillation/arrhythmia 133, 134 |
| Insulin receptor β | Diabetes (Type 2)168, 169 |
| Insulin receptor substrate 1 | Diabetes (Type 2)168, 169 |
| Akt (protein kinase B) | Diabetes (Type 2)14, 168, 169 |
Examples of proteins for which hypo- or hyper-S-nitrosylation has been implicated in the mechanism of disease. Note in addition that S-nitrosylation of multiple substrates including Cox2, Hif-1α, the L-type Ca2+ channel, RyR2 and SERCA2 is implicated in the cardio-protective effects of both statins and ischemia-or drug-induced preconditioning, and in amelioration of the effects of myocardial infarction (see text).