ArticleJournal of cardiovascular pharmacology2011
Thioredoxin reductase inhibition reduces relaxation by increasing oxidative stress and s-nitrosylation in mouse aorta.
Article in Journal of cardiovascular pharmacology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 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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Who cites it
14 citing papers in PubMed, 26 citations in OpenAlex.
- Selenium, a Micronutrient That Modulates Cardiovascular Health via Redox Enzymology.Nutrients · 2021Review
- Redox Switches Controlling Nitric Oxide Signaling in the Resistance Vasculature and Implications for Blood Pressure Regulation: Mid-Career Award for Research Excellence 2020.Hypertension (Dallas, Tex. : 1979) · 2021Review
- Biological Mechanisms ofAntioxidants (Basel, Switzerland) · 2021Review
- The role of the thioredoxin/thioredoxin reductase system in the metabolic syndrome: towards a possible prognostic marker?Cellular and molecular life sciences : CMLS · 2018Review
- Guanylyl cyclase sensitivity to nitric oxide is protected by a thiol oxidation-driven interaction with thioredoxin-1.The Journal of biological chemistry · 2017Article
- Thiol-Based Redox Modulation of Soluble Guanylyl Cyclase, the Nitric Oxide Receptor.Antioxidants & redox signaling · 2017Review
- Identification of novel S-nitrosation sites in soluble guanylyl cyclase, the nitric oxide receptor.Journal of proteomics · 2016Article
- S-nitrosation of proteins relevant to Alzheimer's disease during early stages of neurodegeneration.Proceedings of the National Academy of Sciences of the United States of America · 2016Article
- Induction of Thioredoxin Reductase 1 by Korean Red Ginseng Water Extract Regulates Cytoprotective Effects on Human Endothelial Cells.Evidence-based complementary and alternative medicine : eCAM · 2015Article
- Diet-dependent modulation of gastro-oesphageal vagal afferent mechanosensitivity by endogenous nitric oxide.The Journal of physiology · 2014Article
- Regulation of soluble guanylate cyclase by matricellular thrombospondins: implications for blood flow.Frontiers in physiology · 2014Review
- Cardiovascular redox and ox stress proteomics.Antioxidants & redox signaling · 2012Review
- Augmented S-nitrosylation contributes to impaired relaxation in angiotensin II hypertensive mouse aorta: role of thioredoxin reductase.Journal of hypertension · 2011Article
- Maturation, inactivation, and recovery mechanisms of soluble guanylyl cyclase.The Journal of biological chemistryReview
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
Oxidative stress is well known to lead to vascular dysfunction. Thioredoxin reductase (TrxR) catalyzes the reduction of oxidized thioredoxin. Reduced thioredoxin plays a role in cellular antioxidative defense and in decreasing S-nitrosylation. It is not known whether TrxR affects vascular reactivity. We hypothesized that TrxR inhibition decreases vascular relaxation via increased oxidative stress and S-nitrosylation. Aortic rings from C57BL/6 mice were treated with the TrxR inhibitor, 1-chloro-2,4-dinitrobenzene (DNCB), or auranofin for 30 minutes. Vascular relaxation to acetylcholine was measured in the rings contracted with phenylephrine. DNCB and auranofin reduced relaxation compared with vehicle (vehicle Emax = 71 ± 3%, DNCB Emax = 53 ± 3%; P < 0.05). The antioxidants, apocynin (nicotinamide adenine dinucleotide phosphate oxidase inhibitor), and tempol (superoxide dismutase mimetic) normalized impaired relaxation by DNCB in aorta (DNCB Emax = 53 ± 3%, DNCB + tempol Emax = 66 ± 3%; P < 0.05). In addition, DNCB reduced sodium nitroprusside-induced relaxation. DNCB increased soluble guanylyl cyclase (sGC) S-nitrosylation and decreased sGC activity. These data suggest that TrxR regulates vascular relaxation via antioxidant defense and sGC S-nitrosylation. TrxR may be an enzyme to approach for treatment of vascular dysfunction and arterial hypertension.
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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.