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ROS signaling and redox biology in endothelial cells
Open accessAbstract
The purpose of this review is to provide an overview of redox mechanisms, sources and antioxidants that control signaling events in ECs. In particular, we describe which molecules are involved in redox signaling and how they influence the relationship between ECs and other vascular component with regard to angiogenesis. Recent and new tools to investigate physiological ROS signaling will be also discussed. Such findings are providing an overview of the ROS biology relevant for endothelial cells in the context of normal and pathological angiogenic conditions.
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“NOX5 also appears to modulate proliferation and cell migration processes (371, 719).”
From Sources of Vascular Nitric Oxide and Reactive Oxygen Species and Their Regulation (2019) · cites this paper as [719]
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“Indeed, in some cases, NOXs-dependent ROS formation has been shown to promote cellular adaptation to physical forces and vascular protection during physiological mechano-stress (laminar shear stress) [8] while conversely disturbed blood flow (turbulent flow, oscillatory high rates) or extensive stretch has been associ…”
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ROS homeostasis and metabolism: a dangerous liason in cancer cells
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Metadata
- Authors
- Panieri, E., & Santoro, M. M.
- Affiliations
- University of Turin (IT)
- Vlaams Instituut voor Biotechnologie (BE)
- Corresponding author
- Santoro, Massimo M.
- Venue
- Cellular and Molecular Life Sciences
- Published
- 2015-05-14
- Volume
- 72
- Issue
- 17
- Pages
- 3281-3303
- ISSN
- 1420-682X (ISSN-L)
- 1420-9071
- PMC
- PMC11113497
- OpenAlex
- W347357337
- Cited by
- 168
- References
- 261
- Citations by year
- 2026: 21 · 2025: 10 · 2024: 9 · 2023: 17 · 2022: 13 · 2021: 17 · 2020: 15 · 2019: 15 · 2018: 14 · 2017: 14 · 2016: 20 · 2015: 2
- FWCI
- 1.61
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Cellular and Molecular Life Sciences (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Institutional Research Information System University of Turin (University of Turin) (submittedVersion)
- Padua Research Archive (University of Padova) (submittedVersion)
- Zenodo (CERN European Organization for Nuclear Research) (submittedVersion, other-oa)
- Funders
- Fondazione Telethon (GGP10195)
- European Research Council (CoG - 647057)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Redox biology and oxidative stress
- Health Sciences › Medicine › Physiology (medical) › Nitric Oxide and Endothelin Effects
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Angiogenesis and VEGF in Cancer
- Keywords
- reactive oxygen species, redox signaling, endothelial cells, antioxidants, angiogenesis, oxidative stress, vascular component
- MeSH terms
- Animals, Humans, Mitochondria, Oxidation-Reduction, Signal Transduction, Protein Tyrosine Phosphatases, Reactive Oxygen Species, Neovascularization, Physiologic, NADPH Oxidases, Endothelial Cells
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
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