ArticleDoklady. Biochemistry and biophysics2019
Natural Dicarbonyls Inhibit Peroxidase Activity of Peroxiredoxins.
Article in Doklady. Biochemistry and biophysics, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 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.
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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
5 citing papers in PubMed, 13 citations in OpenAlex.
- Methylglyoxal Formation-Metabolic Routes and Consequences.Antioxidants (Basel, Switzerland) · 2025Review
- The Role of Natural Low Molecular Weight Dicarbonyls in Atherogenesis and Diabetogenesis.Reviews in cardiovascular medicine · 2024Review
- Malondialdehyde as an Important Key Factor of Molecular Mechanisms of Vascular Wall Damage under Heart Diseases Development.International journal of molecular sciences · 2022Review
- Dicarbonyl-Dependent Modification of LDL as a Key Factor of Endothelial Dysfunction and Atherosclerotic Vascular Wall Damage.Antioxidants (Basel, Switzerland) · 2022Review
- MicroRNA-301a-3p increases oxidative stress, inflammation and apoptosis in ox-LDL-induced HUVECs by targeting KLF7.Experimental and therapeutic medicine · 2021Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
It was established that recombinant human peroxiredoxins (Prx1, Prx2, Prx4, and Prx6) inhibit natural dicarbonyls formed during free radical peroxidation of unsaturated lipids (malonic dialdehyde) and oxidative transformations of glucose (glyoxal and methylglyoxal). A possible role of the decrease in the activity of peroxiredoxins under oxidative and carbonyl stress is discussed as an important factor that triggers the molecular mechanisms of vascular wall damage in atherosclerosis and diabetes mellitus.
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Registered trials
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