Nitric oxide‐mediated protein modification in cardiovascular physiology and pathology

Nitric oxide (NO) is a key regulator of cardiovascular functions including the control of vascular tone, anti-inflammatory properties of the endothelium, cardiac contractility, and thrombocyte activation and aggregation. Numerous experimental data support the view that NO not only acts via cyclic guanosine monophosphate (cGMP)-dependent mechanisms but also modulates protein function by nitrosation, nitrosylation, glutathiolation, and nitration, respectively. To understand how NO regulates all of these diverse biological processes on the molecular level a comprehensive assessment of NO-mediated cGMP-dependent and independent targets is required. Novel proteomic approaches allow the simultaneous identification of large quantities of proteins modified in an NO-dependent manner and thereby will considerably deepen our understanding of the role NO plays in cardiovascular physiology and pathophysiology.