Linking RAGE and Nox in diabetic micro- and macrovascular complications

Research output: Contribution to journalReview ArticleResearchpeer-review

25 Citations (Scopus)

Abstract

Diabetes-associated micro- and macrovascular complications contribute to the increased morbidity and mortality observed in diabetes. Diabetes leads to accelerated generation of advanced glycation end products (AGEs) and activation of their receptor, RAGE, as well as activation of NAD(P)H oxidase (Nox), an enzyme dedicated to the production of reactive oxygen species, which ultimately leads to a pro-inflammatory environment characterised by oxidative stress. This review outlines the current evidence about the contribution of and interaction between the AGE-RAGE axis and Nox derived ROS formation in the development and progression of micro- and macrovascular diabetic complications (especially in atherosclerosis and nephropathy), and the mechanisms by which this occurs. We also outline novel treatments targeting the AGE-RAGE axis and specific Nox isoforms, which hold great promise in attenuating the development of diabetes-associated atherosclerosis and diabetic nephropathy.

Original languageEnglish
Pages (from-to)272-281
Number of pages10
JournalDiabetes and Metabolism
Volume41
Issue number4
DOIs
Publication statusPublished - 1 Sep 2015

Keywords

  • Atherosclerosis
  • Diabetes mellitus
  • Glycation
  • NADPH oxidases
  • Nephropathy
  • Oxidative stress
  • RAGE
  • Vascular complications

Cite this

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title = "Linking RAGE and Nox in diabetic micro- and macrovascular complications",
abstract = "Diabetes-associated micro- and macrovascular complications contribute to the increased morbidity and mortality observed in diabetes. Diabetes leads to accelerated generation of advanced glycation end products (AGEs) and activation of their receptor, RAGE, as well as activation of NAD(P)H oxidase (Nox), an enzyme dedicated to the production of reactive oxygen species, which ultimately leads to a pro-inflammatory environment characterised by oxidative stress. This review outlines the current evidence about the contribution of and interaction between the AGE-RAGE axis and Nox derived ROS formation in the development and progression of micro- and macrovascular diabetic complications (especially in atherosclerosis and nephropathy), and the mechanisms by which this occurs. We also outline novel treatments targeting the AGE-RAGE axis and specific Nox isoforms, which hold great promise in attenuating the development of diabetes-associated atherosclerosis and diabetic nephropathy.",
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Linking RAGE and Nox in diabetic micro- and macrovascular complications. / Koulis, C.; Watson, A. M D; Gray, S. P.; Jandeleit-Dahm, K. A.

In: Diabetes and Metabolism, Vol. 41, No. 4, 01.09.2015, p. 272-281.

Research output: Contribution to journalReview ArticleResearchpeer-review

TY - JOUR

T1 - Linking RAGE and Nox in diabetic micro- and macrovascular complications

AU - Koulis, C.

AU - Watson, A. M D

AU - Gray, S. P.

AU - Jandeleit-Dahm, K. A.

PY - 2015/9/1

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N2 - Diabetes-associated micro- and macrovascular complications contribute to the increased morbidity and mortality observed in diabetes. Diabetes leads to accelerated generation of advanced glycation end products (AGEs) and activation of their receptor, RAGE, as well as activation of NAD(P)H oxidase (Nox), an enzyme dedicated to the production of reactive oxygen species, which ultimately leads to a pro-inflammatory environment characterised by oxidative stress. This review outlines the current evidence about the contribution of and interaction between the AGE-RAGE axis and Nox derived ROS formation in the development and progression of micro- and macrovascular diabetic complications (especially in atherosclerosis and nephropathy), and the mechanisms by which this occurs. We also outline novel treatments targeting the AGE-RAGE axis and specific Nox isoforms, which hold great promise in attenuating the development of diabetes-associated atherosclerosis and diabetic nephropathy.

AB - Diabetes-associated micro- and macrovascular complications contribute to the increased morbidity and mortality observed in diabetes. Diabetes leads to accelerated generation of advanced glycation end products (AGEs) and activation of their receptor, RAGE, as well as activation of NAD(P)H oxidase (Nox), an enzyme dedicated to the production of reactive oxygen species, which ultimately leads to a pro-inflammatory environment characterised by oxidative stress. This review outlines the current evidence about the contribution of and interaction between the AGE-RAGE axis and Nox derived ROS formation in the development and progression of micro- and macrovascular diabetic complications (especially in atherosclerosis and nephropathy), and the mechanisms by which this occurs. We also outline novel treatments targeting the AGE-RAGE axis and specific Nox isoforms, which hold great promise in attenuating the development of diabetes-associated atherosclerosis and diabetic nephropathy.

KW - Atherosclerosis

KW - Diabetes mellitus

KW - Glycation

KW - NADPH oxidases

KW - Nephropathy

KW - Oxidative stress

KW - RAGE

KW - Vascular complications

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