title: Hemodynamic regulation of reactive oxygen species: implications for vascular diseases.
abstract: CONCLUSIONS
  Arterial blood vessels functionally and structurally adapt to altering hemodynamic forces in order to accommodate changing needs and to provide stress homeostasis. This ability is achieved at the cellular level by converting mechanical stimulation into biochemical signals (i.e., mechanotransduction). Physiological mechanical stress helps maintain vascular structure and function, whereas pathologic or aberrant stress may impair cellular mechano-signaling, and initiate or augment cellular processes that drive disease.
  
  
  BACKGROUND
  Reactive oxygen species (ROS) may represent an intriguing class of mechanically regulated second messengers. Chronically enhanced ROS generation may be induced by adverse mechanical stresses, and is associated with a multitude of vascular diseases. Although a causal relationship has clearly been demonstrated in large numbers of animal studies, an effective ROS-modulating therapy still remains to be established by clinical studies.
  
  
  CONCLUSIONS
  This review article focuses on the role of various mechanical forces (in the form of laminar shear stress, oscillatory shear stress, or cyclic stretch) as modulators of ROS-driven signaling, and their subsequent effects on vascular biology and homeostasis, as well as on specific diseases such as arteriosclerosis, hypertension, and abdominal aortic aneurysms. Specifically, it highlights the significance of the various NADPH oxidase (NOX) isoforms as critical ROS generators in the vasculature. Directed targeting of defined components in the complex network of ROS (mechano-)signaling may represent a key for successful translation of experimental findings into clinical practice.
authors.affiliation: 1 Division of Cardiovascular Medicine, Stanford University School of Medicine , Stanford, California.
authors.forename: Uwe
authors.initials: U
authors.lastname: Raaz
authors.forename: Ryuji
authors.initials: R
authors.lastname: Toh
authors.forename: Lars
authors.initials: L
authors.lastname: Maegdefessel
authors.forename: Matti
authors.initials: M
authors.lastname: Adam
authors.forename: Futoshi
authors.initials: F
authors.lastname: Nakagami
authors.forename: Fabian C
authors.initials: FC
authors.lastname: Emrich
authors.forename: Joshua M
authors.initials: JM
authors.lastname: Spin
authors.forename: Philip S
authors.initials: PS
authors.lastname: Tsao
mesh_terms: D000818:Animals; D006439:Hemodynamics / Q000502:physiology*; D006801:Humans; D017382:Reactive Oxygen Species / Q000378:metabolism*; D013314:Stress, Mechanical; D014652:Vascular Diseases / Q000378:metabolism* / Q000503:physiopathology
chemical_list: D017382:Reactive Oxygen Species