ReviewJournal of cardiovascular pharmacology2016
Endothelial Cell Redox Regulation of Ischemic Angiogenesis.
Review in Journal of cardiovascular pharmacology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
10 citing papers in PubMed, 17 citations in OpenAlex.
- Regenerative Approach for Improving Flap Survival: Perspective of Angiogenesis.Biomimetics (Basel, Switzerland) · 2026Review
- Microcirculatory failure after successful recanalization in ischemic stroke: insights into mechanisms, imaging, and therapeutic strategies.Frontiers in pharmacology · 2026Review
- Evaluating the Vascular Risk of PFCs: An Integrated XGBoost-Driven Structure-Activity Prediction and Experimental Validation Study.Environment & health (Washington, D.C.) · 2025Article
- Pretreatment with platelet-rich plasma protects against ischemia-reperfusion induced flap injury by deactivating the JAK/STAT pathway in mice.Molecular medicine (Cambridge, Mass.) · 2024Article
- Loss of Id3 (Inhibitor of Differentiation 3) Increases the Number of IgM-Producing B-1b Cells in Ischemic Skeletal Muscle Impairing Blood Flow Recovery During Hindlimb Ischemia.Arteriosclerosis, thrombosis, and vascular biology · 2022Article
- The Role of Sirtuin-1 in the Vasculature: Focus on Aortic Aneurysm.Frontiers in physiology · 2020Review
- Reactive species-induced microvascular dysfunction in ischemia/reperfusion.Free radical biology & medicine · 2019Review
- Endogenous reduction of miR-185 accelerates cardiac function recovery in mice following myocardial infarction via targeting of cathepsin K.Journal of cellular and molecular medicine · 2019Article
- Protein disulfide isomerase regulation by nitric oxide maintains vascular quiescence and controls thrombus formation.Journal of thrombosis and haemostasis : JTH · 2018Article
- Redox regulation of ischemic limb neovascularization - What we have learned from animal studies.Redox biology · 2017Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
13 authors at 1 institution in 1 country.
Funding
Abstract
The endothelium produces and responds to reactive oxygen and nitrogen species (RONS), providing important redox regulation to the cardiovascular system in physiology and disease. In no other situation are RONS more critical than in the response to tissue ischemia. Here, tissue healing requires growth factor-mediated angiogenesis that is in part dependent on low levels of RONS, which paradoxically must overcome the damaging effects of high levels of RONS generated as a result of ischemia. Although the generation of endothelial cell RONS in hypoxia/reoxygenation is acknowledged, the mechanism for their role in angiogenesis is still poorly understood. During ischemia, the major low molecular weight thiol glutathione (GSH) reacts with RONS and protein cysteines, producing GSH-protein adducts. Recent data indicate that GSH adducts on certain proteins are essential to growth factor responses in endothelial cells. Genetic deletion of the enzyme glutaredoxin-1, which selectively removes GSH protein adducts, improves, whereas its overexpression impairs revascularization of the ischemic hindlimb of mice. Ischemia-induced GSH adducts on specific cysteine residues of several proteins, including p65 NF-kB and the sarcoplasmic reticulum calcium ATPase 2, evidently promote ischemic angiogenesis. Identifying the specific proteins in the redox response to ischemia has provided therapeutic opportunities to improve clinical outcomes of ischemia.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.