ReviewAntioxidants & redox signaling2009
Redox-dependent mechanisms in coronary collateral growth: the "redox window" hypothesis.
Review in Antioxidants & redox signaling, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
40 citing papers in PubMed.
- Class I and II Histone Deacetylase Inhibitors as Therapeutic Modulators of Dilated Cardiac Tissue-Derived Mesenchymal Stem/Stromal Cells.International journal of molecular sciences · 2024Article
- Vitamin C as Scavenger of Reactive Oxygen Species during Healing after Myocardial Infarction.International journal of molecular sciences · 2024Review
- The bridge between cell survival and cell death: reactive oxygen species-mediated cellular stress.EXCLI journal · 2023Review
- Reactive Oxygen Species and Oxidative Stress in Vascular-Related Diseases.Oxidative medicine and cellular longevity · 2022Review
- Tuning the intentional corona of cerium oxide nanoparticles to promote angiogenesis via fibroblast growth factor 2 signalling.Regenerative biomaterials · 2022Article
- Natural Herbal Medicine as a Treatment Strategy for Myocardial Infarction through the Regulation of Angiogenesis.Evidence-based complementary and alternative medicine : eCAM · 2022Review
- The role of oxidative stress in patients with recurrent pregnancy loss: a review.Reproductive health · 2021Review
- Article
- Interplay Between Reactive Oxygen/Reactive Nitrogen Species and Metabolism in Vascular Biology and Disease.Antioxidants & redox signaling · 2021Review
- Coronary microvascular adaptations distal to epicardial artery stenosis.American journal of physiology. Heart and circulatory physiology · 2021Review
- Coronary remodeling and biomechanics: Are we going with the flow in 2020?American journal of physiology. Heart and circulatory physiology · 2021Review
- Role of Phytochemicals in Perturbation of Redox Homeostasis in Cancer.Antioxidants (Basel, Switzerland) · 2021Review
- NRF2 activation with Protandim attenuates salt-induced vascular dysfunction and microvascular rarefaction.Microcirculation (New York, N.Y. : 1994) · 2019Article
- Association between Vascular Endothelial Growth Factor Plasma Levels and rs699947 Polymorphism and Coronary Collateral Vessel Formation.The journal of Tehran Heart Center · 2019Article
- The Tri-phasic Role of Hydrogen Peroxide in Blood-Brain Barrier Endothelial cells.Scientific reports · 2019Article
- Blocking LPA-dependent signaling increases ovarian cancer cell death in response to chemotherapy.Redox biology · 2018Article
- PGC-1α (Peroxisome Proliferator-Activated Receptor γ Coactivator 1-α) Overexpression in Coronary Artery Disease Recruits NO and Hydrogen Peroxide During Flow-Mediated Dilation and Protects Against Increased Intraluminal Pressure.Hypertension (Dallas, Tex. : 1979) · 2017Article
- Cardiovascular function in male and female JCR:LA-cp rats: effect of high-fat/high-sucrose diet.American journal of physiology. Heart and circulatory physiology · 2017Article
- Regulation of Coronary Blood Flow.Comprehensive Physiology · 2017Review
- Elevated 20-HETE impairs coronary collateral growth in metabolic syndrome via endothelial dysfunction.American journal of physiology. Heart and circulatory physiology · 2017Article
Corrections and comments
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Authors and funding
7 authors.
Funding
Abstract
This review addresses the complexity of coronary collateral growth from the aspect of redox signaling and introduces the concept of a "redox window" in the context of collateral growth. In essence, the redox window constitutes a range in the redox state of cells, which not only is permissive for the actions of growth factors but also amplifies their actions. The interactions of redox-dependent signaling with growth factors are well established through the actions of many redox-dependent kinases (e.g., Akt and p38 mitogen-activated protein kinase). The initial changes in cellular redox can be induced by a variety of events, from the oxidative burst during reperfusion after ischemia, to recruitment of various types of inflammatory cells capable of producing reactive oxygen species. Any event that "upsets" the normal redox equilibrium is capable of amplifying growth. However, extremes of the redox window, oxidative and reductive stresses, are associated with diminished growth-factor signaling and reduced activation of redox-dependent kinases. This concept of a redox window helps to explain why the clinical trials aimed at stimulating coronary collateral growth, the "therapeutic angiogenesis trials," failed. However, understanding of redox signaling in the context of coronary collateral growth could provide new paradigms for stimulating collateral growth in patients.
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Registered trials
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