Endothelial cell superoxide generation: regulation and relevance for cardiovascular pathophysiology

Li, Jian-Mei; Shah, Ajay M

doi:10.1152/ajpregu.00124.2004

Cited by 773Nitric Oxide and Endothelin EffectsRedox biology and oxidative stressNeutrophil, Myeloperoxidase and Oxidative Mechanisms

Endothelial cell superoxide generation: regulation and relevance for cardiovascular pathophysiology

Li, Jian-Mei, Shah, Ajay M·2004·American Journal of Physiology-Regulatory, Integrative and Comparative Physiology

DOI 10.1152/ajpregu.00124.2004

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Abstract

The endothelial generation of reactive oxygen species (ROS) is important both physiologically and in the pathogenesis of many cardiovascular disorders. ROS generated by endothelial cells include superoxide (O 2−·), hydrogen peroxide (H 2 O 2), peroxynitrite (ONOO−·), nitric oxide (NO), and hydroxyl (·OH) radicals. The O 2−· radical, the focus of the current review, may have several effects either directly or through the generation of other radicals, e.g., H 2 O 2 and ONOO−·. These effects include 1) rapid inactivation of the potent signaling molecule and endothelium-derived relaxing factor NO, leading to endothelial dysfunction; 2) the mediation of signal transduction leading to altered gene transcription and protein and enzyme activities (“redox signaling”); and 3) oxidative damage. Multiple enzymes can generate O 2−·, notably xanthine oxidase, uncoupled NO synthase, and mitochondria. Recent studies indicate that a major source of endothelial O 2−· involved in redox signaling is a multicomponent phagocyte-type NADPH oxidase that is subject to specific regulation by stimuli such as oscillatory shear stress, hypoxia, angiotensin II, growth factors, cytokines, and hyperlipidemia. Depending on the level of oxidants generated and the relative balance between pro- and antioxidant pathways, ROS may be involved in cell growth, hypertrophy, apoptosis, endothelial activation, and adhesivity, for example, in diabetes, hypertension, atherosclerosis, heart failure, and ischemia-reperfusion. This article reviews our current knowledge regarding the sources of endothelial ROS generation, their regulation, their involvement in redox signaling, and the relevance of enhanced ROS generation and redox signaling to the pathophysiology of cardiovascular disorders where endothelial activation and dysfunction are implicated.

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Incomplete reduction of molecular oxygen to superoxide occurs as a result of electron leak during normal respiration in mitochondrial electron transport chain complexes or by enzymatic reduction of molecular oxygen.
“This incomplete reduction reaction occurs as a result of electron leak during normal respiration in the mitochondrial electron transport chain (ETC) complexes or by enzymatic reduction of molecular oxygen (249, 399).”
From Redox regulation of mitochondrial function (2012) · cites this paper as [249]

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Authors: Li, J.-M., & Shah, A. M.
Affiliations: King's College London (GB)
ORCID: Li, Jian-Mei
Shah, Ajay M
Venue: American Journal of Physiology-Regulatory, Integrative and Comparative Physiology
Publisher: American Physiological Society
Published: 2004-11
Volume: 287
Issue: 5
Pages: R1014-R1030
ISSN: 0363-6119 (ISSN-L)
1522-1490
DOI: 10.1152/ajpregu.00124.2004
OpenAlex: W2006847107
Cited by: 773
References: 191
Citations by year: 2026: 5 · 2025: 10 · 2024: 19 · 2023: 11 · 2022: 20 · 2021: 25 · 2020: 20 · 2019: 17 · 2018: 21 · 2017: 21 · 2016: 38 · 2015: 31 · 2014: 39 · 2013: 36 · 2012: 57
FWCI: 35.87
Type: journal article
Language: en
Open access: closed
Locations: American Journal of Physiology-Regulatory, Integrative and Comparative Physiology (publishedVersion)
PubMed (publishedVersion)
Research Portal (King's College London) (submittedVersion)
Topics: Health Sciences › Medicine › Physiology › Nitric Oxide and Endothelin Effects
Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Redox biology and oxidative stress
Life Sciences › Immunology and Microbiology › Immunology › Neutrophil, Myeloperoxidase and Oxidative Mechanisms
Keywords: reactive oxygen species, redox signaling, endothelial dysfunction, NADPH oxidase, xanthine oxidase, uncoupled nitric oxide synthase, mitochondrial superoxide, nitric oxide inactivation, oxidative stress, endothelial activation, shear stress, hypoxia, angiotensin II, hyperlipidemia, atherosclerosis, hypertension, diabetes mellitus, heart failure, ischemia-reperfusion
MeSH terms: Animals, Cardiovascular Diseases, Cardiovascular Physiological Phenomena, Homeostasis, Humans, Inflammation, Oxidation-Reduction, Oxygen Consumption, Superoxides, Signal Transduction, Apoptosis, NADPH Oxidases, Endothelial Cells

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Endothelial cell superoxide generation: regulation and relevance for cardiovascular pathophysiology

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