Nitric oxide and mitochondria in metabolic syndrome
MetadataShow full item record
CitationLitvinova, Larisa, Dmitriy N. Atochin, Nikolai Fattakhov, Mariia Vasilenko, Pavel Zatolokin, and Elena Kirienkova. 2015. “Nitric oxide and mitochondria in metabolic syndrome.” Frontiers in Physiology 6 (1): 20. doi:10.3389/fphys.2015.00020. http://dx.doi.org/10.3389/fphys.2015.00020.
AbstractMetabolic 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 disorders and therefore are highlighted here. Reduced endothelial NOS activity and NO bioavailability, as the main factors underlying the endothelial dysfunction that occurs in MS, are discussed in this review in relation to mitochondrial dysfunction. We also focus on potential therapeutic strategies involving NO signaling pathways that can be used to treat patients with metabolic disorders associated with mitochondrial dysfunction. The article may help researchers develop new approaches for the diagnosis, prevention and treatment of MS.
Citable link to this pagehttp://nrs.harvard.edu/urn-3:HUL.InstRepos:14351380
- HMS Scholarly Articles 
Showing items related by title, author, creator and subject.
Breton, Carrie V.; Salam, Muhammad T.; Wang, Xinhui; Byun, Hyang-Min; Siegmund, Kimberly D.; Gilliland, Frank D. (National Institute of Environmental Health Sciences, 2012)Background: Air pollutants have been associated with childhood asthma and wheeze. Epigenetic regulation of nitric oxide synthase—the gene responsible for nitric oxide production—may be affected by air pollutants and ...
Protective effects of nitric oxide synthase 3 and soluble guanylate cyclase on the outcome of cardiac arrest and cardiopulmonary resuscitation in mice* Nishida, Takefumi; De Yu, Jia; Minamishima, Shizuka; Sips, Patrick; Searles, Robert J.; Buys, Emmanuel; Janssens, Stefan; Brouckaert, Peter; Bloch, Kenneth Daniel; Ichinose, Fumito (Ovid Technologies (Wolters Kluwer Health), 2009)Objectives: Despite advances in resuscitation methods, survival after out-of-hospital cardiac arrest remains low, at least in part, due to postcardiac arrest circulatory and neurologic failure. To elucidate the role of ...
Toll-like Receptor 4 Signaling Confers Cardiac Protection against Ischemic Injury via Inducible Nitric Oxide Synthase- and Soluble Guanylate Cyclase-dependent Mechanisms Wang, E; Feng, Yan; Zhang, Ming; Zou, Lin; Li, Yan; Buys, Emmanuel; Huang, Peigen; Brouckaert, Peter; Chao, Wei (Ovid Technologies (Wolters Kluwer Health), 2011)Background: Prior administration of a small dose of lipopolysaccharide confers a cardiac protection against ischemia-reperfusion injury. However, the signaling mechanisms that control the protection are incompletely ...