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Abstract
Protein S-nitrosylation constitutes a large part of the ubiquitous influence of nitric
oxide on cellular signal transduction and accumulating evidence indicates important
roles for S-nitrosylation both in normal physiology and in a broad spectrum of human
diseases. Here we review recent findings that implicate S-nitrosylation in cardiovascular,
pulmonary, musculoskeletal and neurological (dys)function, as well as in cancer. The
emerging picture shows that, in many cases, pathophysiology correlates with hypo-
or hyper-S-nitrosylation of specific protein targets rather than a general cellular
insult due to loss of or enhanced nitric oxide synthase activity. In addition, it
is increasingly evident that dysregulated S-nitrosylation can not only result from
alterations in the expression, compartmentalization and/or activity of nitric oxide
synthases, but can also reflect a contribution from denitrosylases, including prominently
the S-nitrosoglutathione (GSNO)-metabolizing enzyme GSNO reductase. Finally, because
exogenous mediators of protein S-nitrosylation or denitrosylation can substantially
affect the development or progression of disease, potential therapeutic agents that
modulate S-nitrosylation could well have broad clinical utility.