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Review article

A causal link between oxidative stress and inflammation in cardiovascular and renal complications of diabetes

Jay C. Jha, Florence Ho, Christopher Dan, Karin Jandeleit-Dahm
Clinical Science Aug 30, 2018, 132 (16) 1811-1836; DOI: 10.1042/CS20171459
Jay C. Jha
Department of Diabetes, Central Clinical School, Monash University, Australia
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Florence Ho
Department of Diabetes, Central Clinical School, Monash University, Australia
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Christopher Dan
Department of Diabetes, Central Clinical School, Monash University, Australia
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Karin Jandeleit-Dahm
Department of Diabetes, Central Clinical School, Monash University, Australia
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  • For correspondence: karin.jandeleit-dahm@monash.edu
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Abstract

Chronic renal and vascular oxidative stress in association with an enhanced inflammatory burden are determinant processes in the development and progression of diabetic complications including cardiovascular disease (CVD), atherosclerosis and diabetic kidney disease (DKD). Persistent hyperglycaemia in diabetes mellitus increases the production of reactive oxygen species (ROS) and activates mediators of inflammation as well as suppresses antioxidant defence mechanisms ultimately contributing to oxidative stress which leads to vascular and renal injury in diabetes. Furthermore, there is increasing evidence that ROS, inflammation and fibrosis promote each other and are part of a vicious connection leading to development and progression of CVD and kidney disease in diabetes.

  • atherosclerosis
  • diabetic complications
  • inflammation
  • nephropathy
  • Oxidative stress
  • Abbreviations

    ACE,
    angiotensin-converting enzyme;
    AngII,
    angiotensin II;
    AOPP,
    advanced oxidation protein product;
    ARB,
    angiotensin type 1 receptor blocker;
    ASMC,
    aortic smooth muscle cell;
    CKD,
    chronic kidney disease;
    EC,
    endothelial cell;
    EMT,
    epithelial–mesenchymal transition;
    eNOS,
    endothelial nitric oxide synthase;
    ESRD,
    end-stage renal disease;
    ETA,
    endothelin A;
    HUVEC,
    human umbilical vein endothelial cell;
    ICAM-1,
    intercellular adhesion molecule-1;
    IDL,
    intermediate-density lipoprotein;
    LDL,
    low-density lipoprotein;
    LOX-1,
    low-density lipoprotein receptor-1;
    MCP-1,
    monocyte chemoattractant protein-1;
    mtROS,
    mitochondrial ROS;
    NF-κB,
    nuclear factor kappa-light-chain-enhancer of activated B cells;
    NO,
    nitric oxide;
    NOD2,
    nucleotide-binding oligomerization domain-containing protein 2;
    NOX,
    NADPH oxidase;
    PFD,
    pirfenidone;
    PKC,
    protein kinase C;
    PTF,
    pentoxifylline;
    RAAS,
    renin–angiotensin–aldosterone system;
    ROS,
    reactive oxygen species;
    STZ,
    streptozotocin;
    VCAM-1,
    vascular cell adhesion molecule-1;
    VLDL,
    very low-density lipoprotein;
    VSMC,
    vascular smooth muscle cell
    • © 2018 The Author(s). Published by Portland Press Limited on behalf of the Biochemical Society
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    August 2018

    Volume: 132 Issue: 16

    Clinical Science: 132 (16)
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    A causal link between oxidative stress and inflammation in cardiovascular and renal complications of diabetes
    Jay C. Jha, Florence Ho, Christopher Dan, Karin Jandeleit-Dahm
    Clinical Science Aug 2018, 132 (16) 1811-1836; DOI: 10.1042/CS20171459
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    A causal link between oxidative stress and inflammation in cardiovascular and renal complications of diabetes
    Jay C. Jha, Florence Ho, Christopher Dan, Karin Jandeleit-Dahm
    Clinical Science Aug 2018, 132 (16) 1811-1836; DOI: 10.1042/CS20171459

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    • Article
      • Abstract
      • Introduction
      • Oxidative stress, inflammation and fibrosis: key pathological mechanisms of diabetic atherosclerosis and kidney disease
      • Mitochondrial dysfunction in atherosclerosis and DKD
      • Agents targeting renal and vascular inflammation and fibrosis in diabetes
      • Antioxidants/ROS lowering agents to combat renovascular complications of diabetes
      • Conclusion
      • Competing Interests
      • Funding
      • References
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    Keywords

    atherosclerosis
    diabetic complications
    inflammation
    nephropathy
    oxidative stress

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