ArticleThe Journal of biological chemistry2001
H(2)O(2)-induced O(2) production by a non-phagocytic NAD(P)H oxidase causes oxidant injury.
Article in The Journal of biological chemistry, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 77 papers.
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Who cites it
77 citing papers in PubMed, 266 citations in OpenAlex.
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- From Flies to Men: ROS and the NADPH Oxidase in Phagocytes.Frontiers in cell and developmental biology · 2021Review
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- Oxidative Stress and Microvessel Barrier Dysfunction.Frontiers in physiology · 2020Review
- HPhysiological reports · 2019Article
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- Protective Role of Polyphenols against Vascular Inflammation, Aging and Cardiovascular Disease.Nutrients · 2018Review
- NOX4 Deletion in Male Mice Exacerbates the Effect of Ethanol on Trabecular Bone and Osteoblastogenesis.The Journal of pharmacology and experimental therapeutics · 2018Article
- Paradoxical cardiotoxicity of intraperitoneally-injected epigallocatechin gallate preparation in diabetic mice.Scientific reports · 2018Article
- Regulation of platelet activation and thrombus formation by reactive oxygen species.Redox biology · 2018Review
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- High glucose-induced p53 phosphorylation contributes to impairment of endothelial antioxidant system.Biochimica et biophysica acta. Molecular basis of disease · 2017Article
- ROS-induced ROS release orchestrated by Nox4, Nox2, and mitochondria in VEGF signaling and angiogenesis.American journal of physiology. Cell physiology · 2017Article
17 more citing papers are in PubMed but not listed here.
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Non-phagocytic NAD(P)H oxidases have been implicated as major sources of reactive oxygen species in blood vessels. These oxidases can be activated by cytokines, thereby generating O(2), which is subsequently converted to H(2)O(2) and other oxidant species. The oxidants, in turn, act as important second messengers in cell signaling cascades. We hypothesized that reactive oxygen species, themselves, can activate the non-phagocytic NAD(P)H oxidases in vascular cells to induce oxidant production and, consequently, cellular injury. The current report demonstrates that exogenous exposure of non-phagocytic cell types of vascular origin (smooth muscle cells and fibroblasts) to H(2)O(2) activates these cell types to produce O(2) via an NAD(P)H oxidase. The ensuing endogenous production of O(2) contributes significantly to vascular cell injury following exposure to H(2)O(2). These results suggest the existence of a feed-forward mechanism, whereby reactive oxygen species such as H(2)O(2) can activate NAD(P)H oxidases in non-phagocytic cells to produce additional oxidant species, thereby amplifying the vascular injury process. Moreover, these findings implicate the non-phagocytic NAD(P)H oxidase as a novel therapeutic target for the amelioration of the biological effects of chronic oxidant stress.
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