Nitric oxide and mitochondria in metabolic syndrome.
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 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.
Laboratory of Immunology and Cellular Biotechnologies, Innovation Park of the Immanuel Kant Baltic Federal University Kaliningrad, Russia.
Larisa
L
Litvinova
Cardiology Division, Department of Medicine, Cardiovascular Research Center, Harvard Medical School, Massachusetts General Hospital Boston, MA, USA.
Dmitriy N
DN
Atochin
Laboratory of Immunology and Cellular Biotechnologies, Innovation Park of the Immanuel Kant Baltic Federal University Kaliningrad, Russia.
Nikolai
N
Fattakhov
Laboratory of Immunology and Cellular Biotechnologies, Innovation Park of the Immanuel Kant Baltic Federal University Kaliningrad, Russia.
Mariia
M
Vasilenko
Department of Reconstructive and Endoscopic Surgery, Kaliningrad Regional Hospital Kaliningrad, Russia.
Pavel
P
Zatolokin
Laboratory of Immunology and Cellular Biotechnologies, Innovation Park of the Immanuel Kant Baltic Federal University Kaliningrad, Russia.
Elena
E
Kirienkova
metabolic syndrome; mitochondrial dysfunction; mitochondrial nitric oxide synthase; nitric oxide; nitric oxide synthase; nitric oxide synthase type I; nitric oxide synthase type II; oxide synthase type III