ReviewCirculation journal : official journal of the Japanese Circulation Society2016
Redox Regulation of Ischemic Angiogenesis - Another Aspect of Reactive Oxygen Species.
Review in Circulation journal : official journal of the Japanese Circulation Society, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers, 1 of them a synthesis that pooled it.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
15 citing papers in PubMed, 1 synthesis or guideline pooled it, 31 citations in OpenAlex.
- Involvement of heat shock proteins HSP70 in the mechanisms of endogenous neuroprotection: the prospect of using HSP70 modulators.Frontiers in cellular neuroscience · 2023Pooled it
- Drivers of cardiovascular disease in metabolic dysfunction-associated steatotic liver disease: the threats of oxidative stress.Frontiers in cardiovascular medicine · 2024Review
- HIF‑1α in myocardial ischemia‑reperfusion injury (Review).Molecular medicine reports · 2021Review
- Overexpression of SERCA2a Alleviates Cardiac Microvascular Ischemic Injury by Suppressing Mfn2-Mediated ER/Mitochondrial Calcium Tethering.Frontiers in cell and developmental biology · 2021Article
- Blood collection technique, anticoagulants and storing temperature have minor effects on the isolation of polymorphonuclear neutrophils.Scientific reports · 2020Article
- Protein S-glutathionylation stimulate adipogenesis by stabilizing C/EBPβ in 3T3L1 cells.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2020Article
- Review
- Reactive species-induced microvascular dysfunction in ischemia/reperfusion.Free radical biology & medicine · 2019Review
- P450 Eicosanoids and Reactive Oxygen Species Interplay in Brain Injury and Neuroprotection.Antioxidants & redox signaling · 2018Article
- ROLE OF THIOLS IN OXIDATIVE STRESS.Current opinion in toxicology · 2018Article
- Cardiac pathophysiology in response to environmental stress: a current review.Current opinion in physiology · 2018Article
- Reactive Oxygen Species as Intracellular Signaling Molecules in the Cardiovascular System.Current cardiology reviews · 2018Review
- Redox regulation of ischemic limb neovascularization - What we have learned from animal studies.Redox biology · 2017Review
- Peripheral artery disease, redox signaling, oxidative stress - Basic and clinical aspects.Redox biology · 2017Review
- Gene Expressions Underlying Mishandled Calcium Clearance and Elevated Generation of Reactive Oxygen Species in the Coronary Artery Smooth Muscle Cells of Chronic Heart Failure Rats.Chinese medical journal · 2017Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Antioxidants are expected to improve cardiovascular disease (CVD) by eliminating oxidative stress, but clinical trials have not shown promising results in chronic CVD. Animal studies have revealed that reactive oxygen species (ROS) exacerbate acute CVDs in which high levels of ROS are observed. However, ROS are also necessary for angiogenesis after ischemia, because ROS not only damage cells but also stimulate the cell signaling required for angiogenesis. ROS affect signaling by protein modifications, especially of cysteine amino acid thiols. Although there are several cysteine modifications, S-glutathionylation (GSH adducts; -SSG), a reversible cysteine modification by glutathione (GSH), plays an important role in angiogenic signal transduction by ROS. Glutaredoxin-1 (Glrx) is an enzyme that specifically removes GSH adducts in vivo. Overexpression of Glrx inhibits, whereas deletion of Glrx improves revascularization after mouse hindlimb ischemia. These studies indicate that increased levels of GSH adducts in ischemic muscle are beneficial in promoting angiogenesis. The underlying mechanism can be explained by multiple targets of S-gluathionylation, which mediate the angiogenic effects in ischemia. Increments in the master angiogenic transcriptional factor, HIF-1α, reduction of the anti-angiogenic factor sFlt1, activation of the endoplasmic reticulum Ca(2+)pump, SERCA, and inhibition of phosphatases may occur as a consequence of enhanced S-glutathionylation in ischemic tissue. In summary, inducing S-glutathionylation by inhibiting Glrx may be a therapeutic strategy to improve ischemic angiogenesis in CVD. (Circ J 2016; 80: 1278-1284).
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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.