title: Redox control of cardiovascular homeostasis by angiotensin II.
abstract: Covalent modification of sulfur-containing amino acids in proteins by reactive oxygen species (ROS) has been attracting attention as a major post-translational modification regulating intracellular signal transduction pathways. Angiotensin II Ang II, a major physiologically active substrate in renin-angiotensin (RAS) system, plays a central role in the pathophysiology of cardiovascular systems. Many evidences show that Ang II activates several signaling pathways via an oxidative modification of proteins by Ang II-induced ROS. Ang II induced ROS production is predominantly regulated by three enzymes: NADPH oxidase, mitochondrial respiratory complex, and nitric oxide synthase (NOS), and each enzyme-generating ROS are found to activate appropriate signaling pathways via selective oxidation of specific proteins. These reactions are negatively regulated by ROS-scavenging enzymes or disulfide bridge reducing enzymes, and functional disorders of these enzymes are found to cause cardiovascular dysfunctions. Thus, the spatial and temporal regulation of oxidative modification of signaling proteins by ROS is essential to maintain cardiovascular homeostasis by Ang II. This review brings in the new aspect in understanding ROS-mediated regulation of cardiovascular homeostasis by Ang II, and provides the possible mechanisms underlying metamorphosis of cardiovascular homeostasis by ROS.
authors.affiliation: Department of Drug Discovery and Evolution, Graduate School of Pharmaceutical Sciences, Kyushu University, 3-1-1 Maidashi, Higashi-ku, Fukuoka 812-8582, Japan.
authors.forename: Caroline
authors.initials: C
authors.lastname: Sunggip
authors.forename: Naoyuki
authors.initials: N
authors.lastname: Kitajima
authors.forename: Motohiro
authors.initials: M
authors.lastname: Nishida
mesh_terms: D000804:Angiotensin II / Q000502:physiology*; D002319:Cardiovascular System / Q000378:metabolism*; D016922:Cellular Senescence; D011905:Genes, ras; D006706:Homeostasis; D006801:Humans; D008928:Mitochondria / Q000502:physiology; D019255:NADPH Oxidases / Q000502:physiology; D052250:Nitric Oxide Synthase Type III / Q000502:physiology; D010084:Oxidation-Reduction; D017382:Reactive Oxygen Species / Q000378:metabolism; D044140:Receptor, Angiotensin, Type 1 / Q000502:physiology; D012084:Renin-Angiotensin System / Q000502:physiology; D015398:Signal Transduction
chemical_list: D017382:Reactive Oxygen Species; D044140:Receptor, Angiotensin, Type 1; D000804:Angiotensin II; D052250:Nitric Oxide Synthase Type III; D019255:NADPH Oxidases