Cited by 636Immune cells in cancerRedox biology and oxidative stressAdipokines, Inflammation, and Metabolic Diseases

Reactive oxygen species (ROS) in macrophage activation and function in diabetes

Open access
Rendra, Erika, Riabov, Vladimir, Mossel, Dieuwertje M., Sevastyanova, Tatyana, Harmsen, Martin C., Kzhyshkowska, Julia·2019·Immunobiology

Abstract

In a diabetic milieu high levels of reactive oxygen species (ROS) are induced. This contributes to the vascular complications of diabetes. Recent studies have shown that ROS formation is exacerbated in diabetic monocytes and macrophages due to a glycolytic metabolic shift. Macrophages are important players in the progression of diabetes and promote inflammation through the release of pro-inflammatory cytokines and proteases. Because ROS is an important mediator for the activation of pro-inflammatory signaling pathways, obesity and hyperglycemia-induced ROS production may favor induction of M1-like pro-inflammatory macrophages during diabetes onset and progression. ROS induces MAPK, STAT1, STAT6 and NFκB signaling, and interferes with macrophage differentiation via epigenetic (re)programming. Therefore, a comprehensive understanding of the impact of ROS on macrophage phenotype and function is needed in order to improve treatment of diabetes and its vascular complications. In the current comprehensive review, we dissect the role of ROS in macrophage polarization, and analyze how ROS production links metabolism and inflammation in diabetes and its complications. Finally, we discuss the contribution of ROS to the crosstalk between macrophages and endothelial cells in diabetic complications.

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Crossref · 10.1016/j.imbio.2018.11.010

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Authors
Rendra, E., Riabov, V., Mossel, D. M., Sevastyanova, T., Harmsen, M. C., & Kzhyshkowska, J.
Affiliations
  • University Medical Center Groningen (NL)
  • National Research Tomsk State University (RU)
  • Heidelberg University (DE)
Corresponding author
Kzhyshkowska, Julia
Venue
Immunobiology
Publisher
Elsevier BV
Published
2019-03
Volume
224
Issue
2
Pages
242-253
ISSN
0171-2985 (ISSN-L)
OpenAlex
W2903169176
Cited by
636
References
147
Citations by year
2026: 66 · 2025: 100 · 2024: 127 · 2023: 117 · 2022: 107 · 2021: 66 · 2020: 42 · 2019: 9 · 2015: 1
FWCI
2.99
Type
journal article
Language
en
Open access
Locations
  • Immunobiology (publishedVersion)
  • PubMed (publishedVersion)
  • University of Groningen research database (University of Groningen / Centre for Information Technology) (publishedVersion, other-oa)
  • University of Groningen research database (University of Groningen / Centre for Information Technology) (submittedVersion, other-oa)
Funders
DFG GRK 1874 DIAMICOM and the Program of increasing the competitiveness of TSU (8.1.23.2018)
Topics
  • Life Sciences › Immunology and Microbiology › Immunology › Immune cells in cancer
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Redox biology and oxidative stress
  • Health Sciences › Medicine › Epidemiology › Adipokines, Inflammation, and Metabolic Diseases
Keywords
reactive oxygen species, macrophage activation, diabetes mellitus, macrophage polarization, M1 macrophages, inflammatory cytokines, NF-κB signaling, MAPK signaling, STAT1, STAT6, epigenetic reprogramming, macrophage differentiation, diabetic vascular complications, hyperglycemia, obesity, inflammation
MeSH terms
Animals, Diabetes Mellitus, Disease Susceptibility, Energy Metabolism, Humans, Macrophage Activation, Macrophages, Signal Transduction, Reactive Oxygen Species, Oxidative Stress, Immunomodulation

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