Oxidative Stress and Hypertension

  • Kathy K. Griendling
    Division of Cardiology, Department of Medicine, Emory University, Atlanta, GA (K.K.G.).
  • Livia L. Camargo
    Institute of Cardiovascular and Medical Sciences, BHF Glasgow Cardiovascular Research Centre, University of Glasgow, United Kingdom (L.L.C., F.J.R., R.A.-L., A.C.M., R.M.T.).
  • Francisco J. Rios
    Institute of Cardiovascular and Medical Sciences, BHF Glasgow Cardiovascular Research Centre, University of Glasgow, United Kingdom (L.L.C., F.J.R., R.A.-L., A.C.M., R.M.T.).
  • Rhéure Alves-Lopes
    Institute of Cardiovascular and Medical Sciences, BHF Glasgow Cardiovascular Research Centre, University of Glasgow, United Kingdom (L.L.C., F.J.R., R.A.-L., A.C.M., R.M.T.).
  • Augusto C. Montezano
    Institute of Cardiovascular and Medical Sciences, BHF Glasgow Cardiovascular Research Centre, University of Glasgow, United Kingdom (L.L.C., F.J.R., R.A.-L., A.C.M., R.M.T.).
  • Rhian M. Touyz
    Institute of Cardiovascular and Medical Sciences, BHF Glasgow Cardiovascular Research Centre, University of Glasgow, United Kingdom (L.L.C., F.J.R., R.A.-L., A.C.M., R.M.T.).

抄録

<jats:p>A link between oxidative stress and hypertension has been firmly established in multiple animal models of hypertension but remains elusive in humans. While initial studies focused on inactivation of nitric oxide by superoxide, our understanding of relevant reactive oxygen species (superoxide, hydrogen peroxide, and peroxynitrite) and how they modify complex signaling pathways to promote hypertension has expanded significantly. In this review, we summarize recent advances in delineating the primary and secondary sources of reactive oxygen species (nicotinamide adenine dinucleotide phosphate oxidases, uncoupled endothelial nitric oxide synthase, endoplasmic reticulum, and mitochondria), the posttranslational oxidative modifications they induce on protein targets important for redox signaling, their interplay with endogenous antioxidant systems, and the role of inflammasome activation and endoplasmic reticular stress in the development of hypertension. We highlight how oxidative stress in different organ systems contributes to hypertension, describe new animal models that have clarified the importance of specific proteins, and discuss clinical studies that shed light on how these processes and pathways are altered in human hypertension. Finally, we focus on the promise of redox proteomics and systems biology to help us fully understand the relationship between ROS and hypertension and their potential for designing and evaluating novel antihypertensive therapies.</jats:p>

収録刊行物

  • Circulation Research

    Circulation Research 128 (7), 993-1020, 2021-04-02

    Ovid Technologies (Wolters Kluwer Health)

被引用文献 (1)*注記

もっと見る

詳細情報 詳細情報について

問題の指摘

ページトップへ