title: Endoplasmic reticulum stress and Nox-mediated reactive oxygen species signaling in the peripheral vasculature: potential role in hypertension.
abstract: CONCLUSIONS
  Reactive oxygen species (ROS) are produced during normal endoplasmic reticulum (ER) metabolism. There is accumulating evidence showing that under stress conditions such as ER stress, ROS production is increased via enzymes of the NADPH oxidase (Nox) family, especially via the Nox2 and Nox4 isoforms, which are involved in the regulation of blood pressure. Hypertension is a major contributor to cardiovascular and renal disease, and it has a complex pathophysiology involving the heart, kidney, brain, vessels, and immune system. ER stress activates the unfolded protein response (UPR) signaling pathway that has prosurvival and proapoptotic components.
  
  
  BACKGROUND
  Here, we summarize the evidence regarding the association of Nox enzymes and ER stress, and its potential contribution in the setting of hypertension, including the role of other conditions that can lead to hypertension (e.g., insulin resistance and diabetes).
  
  
  RESULTS
  A better understanding of this association is currently of great interest, as it will provide further insights into the cellular mechanisms that can drive the ER stress-induced adaptive versus maladaptive pathways linked to hypertension and other cardiovascular conditions. More needs to be learnt about the precise signaling regulation of Nox(es) and ER stress in the cardiovascular system.
  
  
  CONCLUSIONS
  The development of specific approaches that target individual Nox isoforms and the UPR signaling pathway may be important for the achievement of therapeutic efficacy in hypertension.
authors.affiliation: 1 Cardiovascular Division, King's College London British Heart Foundation Centre of Excellence , London, United Kingdom .
authors.forename: Celio X C
authors.initials: CX
authors.lastname: Santos
authors.forename: Adam A
authors.initials: AA
authors.lastname: Nabeebaccus
authors.forename: Ajay M
authors.initials: AM
authors.lastname: Shah
authors.forename: Livia L
authors.initials: LL
authors.lastname: Camargo
authors.forename: Sidney V
authors.initials: SV
authors.lastname: Filho
authors.forename: Lucia R
authors.initials: LR
authors.lastname: Lopes
mesh_terms: D000818:Animals; D001808:Blood Vessels / Q000378:metabolism*; D003920:Diabetes Mellitus / Q000378:metabolism; D059865:Endoplasmic Reticulum Stress; D006801:Humans; D006973:Hypertension / Q000378:metabolism; D007333:Insulin Resistance; D019255:NADPH Oxidases / Q000378:metabolism*; D017382:Reactive Oxygen Species / Q000378:metabolism*; D015398:Signal Transduction
chemical_list: D017382:Reactive Oxygen Species; D019255:NADPH Oxidases