on September 20, 2007
Published online before print September 20, 2007, doi: 10.1161/ATVBAHA.107.151167
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Submitted on July 3, 2007
Accepted on September 13, 2007
Nitric Oxide and Mitochondrial Signaling. From Physiology to Pathophysiology
Jorge D. Erusalimsky * and Salvador Moncada
From The Wolfson Institute for Biomedical Research (J.D.E., S.M.), University College London, and the Cardiff School of Health Sciences (J.D.E.), University of Wales Institute Cardiff, UK.
* To whom correspondence should be addressed. E-mail: apreiner{at}u.washington.edu.
Abstract—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.
Key words: nitric oxide • mitochondria • reactive oxygen species • signal transduction • cytoprotection
This article has been cited by other articles:
 |
|
 |
|
  J. Van Blerkom, P. Davis, and V. Thalhammer Regulation of mitochondrial polarity in mouse and human oocytes: the influence of cumulus derived nitric oxide Mol. Hum. Reprod., August 1, 2008; 14(8): 431 - 444. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 M. Schleicher and W. C. Sessa Are the Mechanisms for NO-Dependent Vascular Remodeling Different From Vasorelaxation In Vivo? Arterioscler. Thromb. Vasc. Biol., July 1, 2008; 28(7): 1207 - 1208. [Full Text] [PDF]
|
|
|
|
 |
|
 N. Lerner-Marmarosh, T. Miralem, P. E. M. Gibbs, and M. D. Maines Human biliverdin reductase is an ERK activator; hBVR is an ERK nuclear transporter and is required for MAPK signaling PNAS, May 13, 2008; 105(19): 6870 - 6875. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 J. Ruttimann Macrophages and nitric oxide: A deadly combination J. Exp. Med., December 24, 2007; 204(13): 3057 - 3057. [Abstract] [Full Text] [PDF]
|
|