ReviewInternational journal of molecular sciences2013
S-glutathionylation in monocyte and macrophage (dys)function.
Review in International journal of molecular sciences, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 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.
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, 29 citations in OpenAlex.
- Crosstalk between Oxidative Stress and Inflammation Caused by Noise and Air Pollution-Implications for Neurodegenerative Diseases.Antioxidants (Basel, Switzerland) · 2024Review
- Plant In Vitro Culture Factories for Pentacyclic Triterpenoid Production.Advances in biochemical engineering/biotechnology · 2024Review
- Macrophage-restricted overexpression of glutaredoxin 1 protects against atherosclerosis by preventing nutrient stress-induced macrophage dysfunction and reprogramming.Atherosclerosis · 2023Article
- Glutaredoxin 1 controls monocyte reprogramming during nutrient stress and protects mice against obesity and atherosclerosis in a sex-specific manner.Nature communications · 2022Article
- Oxidized GAPDH transfers S-glutathionylation to a nuclear protein Sirtuin-1 leading to apoptosis.Free radical biology & medicine · 2021Article
- Ursolic Acid and Related Analogues: Triterpenoids with Broad Health Benefits.Antioxidants (Basel, Switzerland) · 2021Review
- Vascular Inflammation and Oxidative Stress: Major Triggers for Cardiovascular Disease.Oxidative medicine and cellular longevity · 2019Review
- Dietary 23-hydroxy ursolic acid protects against atherosclerosis and obesity by preventing dyslipidemia-induced monocyte priming and dysfunction.Atherosclerosis · 2018Article
- GSTO1-1 plays a pro-inflammatory role in models of inflammation, colitis and obesity.Scientific reports · 2017Article
- Microglia antioxidant systems and redox signalling.British journal of pharmacology · 2017Review
- Aorta macrophage inflammatory and epigenetic changes in a murine model of obstructive sleep apnea: Potential role of CD36.Scientific reports · 2017Article
- Oxidative Stress and Neurobiology of Demyelination.Molecular neurobiology · 2016Review
- Glutaredoxin 2a overexpression in macrophages promotes mitochondrial dysfunction but has little or no effect on atherogenesis in LDL-receptor null mice.Atherosclerosis · 2015Article
- Study of linkage between glutathione pathway and the antibiotic resistance of Escherichia coli from patients' swabs.International journal of molecular sciences · 2015Article
- Redox control of microglial function: molecular mechanisms and functional significance.Antioxidants & redox signaling · 2014Review
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
Atherosclerosis is a chronic inflammatory disease involving the accumulation of monocytes and macrophages in the vascular wall. Monocytes and macrophages play a central role in the initiation and progression of atherosclerotic lesion development. Oxidative stress, which occurs when reactive oxygen species (ROS) overwhelm cellular antioxidant systems, contributes to the pathophysiology of many chronic inflammatory diseases, including atherosclerosis. Major targets of ROS are reactive thiols on cysteine residues in proteins, which when oxidized can alter cellular processes, including signaling pathways, metabolic pathways, transcription, and translation. Protein-S-glutathionylation is the process of mixed disulfide formation between glutathione (GSH) and protein thiols. Until recently, protein-S-glutathionylation was associated with increased cellular oxidative stress, but S-glutathionylation of key protein targets has now emerged as a physiologically important redox signaling mechanism, which when dysregulated contributes to a variety of disease processes. In this review, we will explore the role of thiol oxidative stress and protein-S-glutathionylation in monocyte and macrophage dysfunction as a mechanistic link between oxidative stress associated with metabolic disorders and chronic inflammatory diseases, including atherosclerosis.
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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.