Nitric oxide and mitochondrial signaling: From physiology to pathophysiology

Jorge D. Erusalimsky, Salvador Moncada

    Research output: Contribution to journalArticlepeer-review


    Nitric oxide (NO) has been known for many years to bind to cytochrome C oxidase, the terminal acceptor in the mitochondrial electron transport chain, in competition with oxygen. This interaction may be significant in vivo and explain some of the biological actions of NO. In this article we review the evidence showing that binding of NO to cytochrome C oxidase elicits intracellular signaling events, including the diversion of oxygen to nonrespiratory substrates and the generation of reactive oxygen species. We discuss findings indicating that these NO-elicited events act as triggers by which mitochondria modulate signal transduction cascades involved in the induction of cellular defense mechanisms and adaptive responses. We also discuss instances in which the effects of NO on the electron transport chain might lead to mitochondrial dysfunction and pathology. © 2007 American Heart Association, Inc.
    Original languageEnglish
    Pages (from-to)2524-2531
    Number of pages7
    JournalArteriosclerosis, Thrombosis, and Vascular Biology
    Issue number12
    Publication statusPublished - Dec 2007


    • Cytoprotection
    • Mitochondria
    • Nitric oxide
    • Reactive oxygen species
    • Signal transduction


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