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Cited by 15Nitric Oxide and Endothelin EffectsNeutrophil, Myeloperoxidase and Oxidative MechanismsRedox biology and oxidative stress

Endothelial NADPH oxidase 2: when does it matter in atherosclerosis?

Haendeler, J., Eckers, A., Lukosz, M., Unfried, K., Altschmied, J.·2012·Cardiovascular Research
DOI 10.1093/cvr/cvs106
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Abstract

This editorial refers to ‘Endothelial-specific Nox2 overexpression increases vascular superoxide and macrophage recruitment in ApoE−/− mice’ by G. Douglas et al., pp. 20–29, this issue. Reactive oxygen species (ROS) act as a double-edged sword in numerous cardiovascular conditions. In addition to their known detrimental effects on all cellular macromolecules, referred to as oxidative stress, lower amounts of ROS also directly modify molecules and thereby modulate their functions - this process has been termed redox signalling. Both oxidative stress and redox signalling have been implicated in the process of atherosclerosis. The sources of cellular ROS include mitochondria, NADPH oxidases (Noxs), dysfunctional nitric oxide synthases, xanthine oxidase, and other oxygenases. Among these, the Noxs are unique, since their primary function is to produce ROS.1 The Nox family comprises seven members, Nox1–5 and DUOX1–2, each based on a distinct core catalytic subunit.1,2 Nox1, 2, 4, and 5 are expressed in cardiovascular cells, although Nox5 is only found in humans and not in rodents.3 An involvement of Nox2 in atherosclerosis has been suspected. It was the first NADPH oxidase to be identified and is responsible for the phagocytic oxidative burst of neutrophils. It has subsequently been found to be expressed at lower levels in endothelial cells, cardiomyocytes, fibroblasts, vascular smooth muscle cells, monocytes, and macrophages, the latter two being central players in atherogenesis.4 However, findings in mice with global Nox2 deficiency on an atherosclerosis-prone ApoE−/− genetic background and fed a high-fat diet are contradictory. Kirk et al.5 found no protection against atherosclerosis when examining aortic sinus sections, whereas Judkins et al.6 demonstrated a 50% reduction in lesion area in the region between the aortic arch and iliac bifurcation. However, using global Nox2 deficiency, it is impossible to identify the cell types relevant for atherosclerosis. Thus, it is important to investigate the role of Nox2 in a cell-specific manner.

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  • Macrophage NOX2 is more detrimental in the development of cardiovascular disease.

    “The current paradigm indicates that macrophage NOX2 is more detrimental in the development of cardiovascular disease (395, 876), with endothelial NOX2 probably involved in the initiation, but not so much in the development of the disease, and a subsequent progress of the atherosclerotic lesion dependent on immune cells (243, 573, 976).”

    From Sources of Vascular Nitric Oxide and Reactive Oxygen Species and Their Regulation (2019) · cites this paper as [395]

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Authors
Haendeler, J., Eckers, A., Lukosz, M., Unfried, K., & Altschmied, J.
Affiliations
Leibniz Institute of Environmental Medicine (DE)
Corresponding author
Haendeler, J.
ORCID
Venue
Cardiovascular Research
Publisher
Oxford University Press (OUP)
Published
2012-02-23
Volume
94
Issue
1
Pages
1-2
ISSN
0008-6363 (ISSN-L)
DOI
10.1093/cvr/cvs106
OpenAlex
W2150811169
Cited by
15
References
11
Citations by year
2025: 1 · 2023: 3 · 2021: 2 · 2019: 1 · 2018: 3 · 2017: 1 · 2015: 1 · 2014: 2 · 2013: 1
Type
journal article
Language
en
Open access
closed
Locations
  • Cardiovascular Research (publishedVersion)
  • PubMed (publishedVersion)
Topics
  • Health Sciences › Medicine › Physiology › Nitric Oxide and Endothelin Effects
  • Life Sciences › Immunology and Microbiology › Immunology › Neutrophil, Myeloperoxidase and Oxidative Mechanisms
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Redox biology and oxidative stress
Keywords
NADPH oxidase 2, endothelial cells, atherosclerosis, reactive oxygen species, redox signaling, oxidative stress, macrophage recruitment, superoxide, ApoE-deficient mice, atherosclerotic plaque
MeSH terms
NADPH Oxidase 2, Animals, Aortic Diseases, Apolipoproteins E, Chemotaxis, Humans, Macrophages, Membrane Glycoproteins, Superoxides, NADPH Oxidases, Endothelial Cells, Atherosclerosis

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