ArticleCirculation2013
Vascular injury involves the overoxidation of peroxiredoxin type II and is recovered by the peroxiredoxin activity mimetic that induces reendothelialization.
Article in Circulation, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
What it found
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Who cites it
20 citing papers in PubMed, 32 citations in OpenAlex.
- Smooth Muscle Cell Cytoglobin is a Negative Regulator of Atherosclerotic Fibrous Cap Development.bioRxiv : the preprint server for biology · 2026Article
- Insights into the activation patterns of 1,2-dithiolane unit in biofunctional molecules.Nature communications · 2026Article
- Beyond Antioxidants: How Redox Pathways Shape Cellular Signaling and Disease Outcomes.Antioxidants (Basel, Switzerland) · 2025Review
- Prolonged In Vivo Chemogenetic Generation of Hydrogen Peroxide by Endothelial Cells Induces Cardiac Remodelling and Vascular Dysfunction.Antioxidants (Basel, Switzerland) · 2025Article
- Conserved miR-370-3p/BMP-7 axis regulates the phenotypic change of human vascular smooth muscle cells.Scientific reports · 2023Article
- CFTR Suppresses Neointimal Formation Through Attenuating Proliferation and Migration of Aortic Smooth Muscle Cells.Journal of cardiovascular pharmacology · 2022Article
- Microbe-Derived Butyrate and Its Receptor, Free Fatty Acid Receptor 3, But Not Free Fatty Acid Receptor 2, Mitigate Neointimal Hyperplasia Susceptibility After Arterial Injury.Journal of the American Heart Association · 2020Article
- Knockout Mouse Models for Peroxiredoxins.Antioxidants (Basel, Switzerland) · 2020Review
- Role of smooth muscle cells in Cardiovascular Disease.International journal of biological sciences · 2020Review
- Cancer-Associated Function of 2-Cys Peroxiredoxin Subtypes as a Survival Gatekeeper.Antioxidants (Basel, Switzerland) · 2018Review
- The Multifaceted Impact of Peroxiredoxins on Aging and Disease.Antioxidants & redox signaling · 2018Review
- Cholinergic anti-inflammatory pathway inhibits neointimal hyperplasia by suppressing inflammation and oxidative stress.Redox biology · 2018Article
- Prdx1 (peroxiredoxin 1) deficiency reduces cholesterol efflux via impaired macrophage lipophagic flux.Autophagy · 2018Article
- Proteomic analysis of the human retina reveals region-specific susceptibilities to metabolic- and oxidative stress-related diseases.PloS one · 2018Article
- Endothelial-Vascular Smooth Muscle Cells Interactions in Atherosclerosis.Frontiers in cardiovascular medicine · 2018Review
- Roles of peroxiredoxins in cancer, neurodegenerative diseases and inflammatory diseases.Pharmacology & therapeutics · 2016Review
- Repeated Superovulation via PMSG/hCG Administration Induces 2-Cys Peroxiredoxins Expression and Overoxidation in the Reproductive Tracts of Female Mice.Molecules and cells · 2015Article
- ROS signaling and redox biology in endothelial cells.Cellular and molecular life sciences : CMLS · 2015Review
- Article
- Hyperhomocysteinemia accelerates collagen accumulation in the adventitia of balloon-injured rat carotid arteries via angiotensin II type 1 receptor.International journal of molecular sciences · 2014Article
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 2 countries.
Funding
Abstract
backgroundTypical 2-Cys peroxiredoxin (Prx) is inactivated by overoxidation of the peroxidatic cysteine residue under oxidative stress. However, the significance in the context of vascular disease is unknown. METHODS AND
resultsImmunohistochemical analyses revealed that 2-Cys Prxs, particularly Prx type II, are heavily overoxidized in balloon-injured rodent carotid vessels and in human atherosclerotic lesions. Consistent with this observation, the selective depletion of Prx II exacerbated neointimal hyperplasia in injured carotid vessels. We also found that the epipolythiodioxopiperazine class of fungal metabolites exhibited an enzyme-like activity mimicking 2-Cys Prx peroxidase and manifestly eliminated the intracellular H₂O₂ in the vascular cells. Functionally, the epipolythiodioxopiperazines reciprocally regulated the platelet-derived growth factor receptor-β- and vascular endothelial growth factor receptor-mediated signaling in these vascular cells by replacing Prx II. As a consequence, the epipolythiodioxopiperazines inhibited the proliferative and migratory activities of smooth muscle cells but promoted those of endothelial cells in vitro. Moreover, administration of the epipolythiodioxopiperazines to the injured carotid vessels resulted in a successful recovery by inhibiting neointimal hyperplasia without causing cytotoxicity and simultaneously inducing reendothelialization.
conclusionsThis study reveals for the first time the involvement of the 2-Cys Prx overoxidation and thus the therapeutic use of their activity mimetic in vascular injuries like stenting.
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