2015
DOI: 10.3389/fphys.2015.00020
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Nitric oxide and mitochondria in metabolic syndrome

Abstract: Metabolic syndrome (MS) is a cluster of metabolic disorders that collectively increase the risk of cardiovascular disease. Nitric oxide (NO) plays a crucial role in the pathogeneses of MS components and is involved in different mitochondrial signaling pathways that control respiration and apoptosis. The present review summarizes the recent information regarding the interrelations of mitochondria and NO in MS. Changes in the activities of different NO synthase isoforms lead to the formation of metabolic disorde… Show more

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Cited by 102 publications
(101 citation statements)
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References 90 publications
(98 reference statements)
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“…Alternatively ORC1 and ORC2 might catalyze the heteroexchange of cytoplasmic arginine for matrix citrulline formed by mtNOS. Important roles have been attributed to mitochondrial NO, which may reversibly inhibit cytochrome c oxidase and react with mitochondrial thiol-containing proteins and superoxide anion to produce peroxynitrite as well as to act as a signaling molecule involved in apoptosis and metabolic syndrome (Ghafourifar and Cadenas 2005;Litvinova et al 2015). Arginine may be converted to ornithine in the matrix by arginase II, which is the non-hepatic isoform and is localized in mitochondria, or in the cytosol by arginase I that is mainly expressed in liver (Wu and Morris 1998).…”
Section: Physiological Roles Of Human Orc1 Orc2 and Slc25a29mentioning
confidence: 98%
“…Alternatively ORC1 and ORC2 might catalyze the heteroexchange of cytoplasmic arginine for matrix citrulline formed by mtNOS. Important roles have been attributed to mitochondrial NO, which may reversibly inhibit cytochrome c oxidase and react with mitochondrial thiol-containing proteins and superoxide anion to produce peroxynitrite as well as to act as a signaling molecule involved in apoptosis and metabolic syndrome (Ghafourifar and Cadenas 2005;Litvinova et al 2015). Arginine may be converted to ornithine in the matrix by arginase II, which is the non-hepatic isoform and is localized in mitochondria, or in the cytosol by arginase I that is mainly expressed in liver (Wu and Morris 1998).…”
Section: Physiological Roles Of Human Orc1 Orc2 and Slc25a29mentioning
confidence: 98%
“…Indeed, unbalanced • NO signaling can significantly contribute to pathological events, such as neurodegenerative diseases, inflammation, arthritis, septic shock, diabetes, and cerebral ischemia. [10][11][12] Nitroxyl (azanone, HNO) is a highly reactive protonated • NO congener that has been reported due to its distinct redox chemical and biological properties. Interestingly, many of the properties attributed to • NO may in fact be mediated by HNO.…”
Section: F I G U R E 1 Biological Pathways Of • No Formation and Decomentioning
confidence: 99%
“…The main biological effects of • NO occur in the cardiovascular system, where • NO is continuously produced by the endothelial cells that line the lumen of blood vessels, but it also influences the homeostasis of other organ systems. Indeed, unbalanced • NO signaling can significantly contribute to pathological events, such as neurodegenerative diseases, inflammation, arthritis, septic shock, diabetes, and cerebral ischemia …”
Section: Introductionmentioning
confidence: 99%
“…Different risk factors such as metabolic and genetic components contribute to this emerging health problem. 4,5 Different studies also suggest that increased intake of red meat, fat, sodium, and inadequate use of vegetables and fruits may be the reasons associated with the increased prevalence of metabolic disorders. 6 The pathogenesis and progress of metabolic syndrome also have an association with dietary patterns and nutritional intake.…”
Section: Introductionmentioning
confidence: 99%