ArticleArchives of biochemistry and biophysics2011
Specific antioxidant selenoproteins are induced in the heart during hypertrophy.
Article in Archives of biochemistry and biophysics, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 45 citations in OpenAlex.
- Cardiac redox imbalance upon disruption of selenocysteine decomposition in mice.American journal of physiology. Heart and circulatory physiology · 2025Article
- The redox-active defensive Selenoprotein T as a novel stress sensor protein playing a key role in the pathophysiology of heart failure.Journal of translational medicine · 2024Article
- The Role of Selenoprotein Tissue Homeostasis in MetS Programming: Energy Balance and Cardiometabolic Implications.Antioxidants (Basel, Switzerland) · 2022Review
- Serum Zinc and Selenium Concentrations in Patients with Hypertrophy and Remodelling of the Left Ventricle Secondary to Arterial Hypertension.Antioxidants (Basel, Switzerland) · 2021Article
- The Impact of Selenium Deficiency on Cardiovascular Function.International journal of molecular sciences · 2021Review
- Selenium, a Micronutrient That Modulates Cardiovascular Health via Redox Enzymology.Nutrients · 2021Review
- The Association Between Dietary Antioxidant Micronutrients and Cardiovascular Disease in Adults in the United States: A Cross-Sectional Study.Frontiers in nutrition · 2021Article
- Role of Selenoproteins in Redox Regulation of Signaling and the Antioxidant System: A Review.Antioxidants (Basel, Switzerland) · 2020Review
- Progress in the emerging role of selenoproteins in cardiovascular disease: focus on endoplasmic reticulum-resident selenoproteins.Cellular and molecular life sciences : CMLS · 2019Review
- Oxidative Stress and Neonatal Respiratory Extracorporeal Membrane Oxygenation.Frontiers in physiology · 2018Review
- Dietary Selenium Status Regulates the Transcriptions of Selenoproteome and Activities of Selenoenzymes in Chicken Kidney at Low or Super-nutritional Levels.Biological trace element research · 2016Article
- Obesity in a model of gpx4 haploinsufficiency uncovers a causal role for lipid-derived aldehydes in human metabolic disease and cardiomyopathy.Molecular metabolism · 2015Article
- Review
- Selenoproteins and cardiovascular stress.Thrombosis and haemostasis · 2015Review
- Redox Changes Induced by General Anesthesia in Critically Ill Patients with Multiple Traumas.Molecular biology international · 2015Review
- Article
- Calpastatin prevents NF-κB-mediated hyperactivation of macrophages and attenuates colitis.Journal of immunology (Baltimore, Md. : 1950) · 2013Article
- Article
- Cardiovascular redox and ox stress proteomics.Antioxidants & redox signaling · 2012Review
- CardioNet: a human metabolic network suited for the study of cardiomyocyte metabolism.BMC systems biology · 2012Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
Selenium (Se) is thought to confer cardioprotective effects through the actions of antioxidant selenoprotein enzymes that directly limit levels of ROS such as hydrogen peroxide (H(2)O(2)) or that reverse oxidative damage to lipids and proteins. To determine how the selenoproteome responds to myocardial hypertrophy, two mouse models were employed: triidothyronine (T3)- or isoproterenol (ISO)-treatment. After 7days of T3- and ISO-treatment, cardiac stress was demonstrated by increased H(2)O(2) and caspase-3 activity. Neither treatment produced significant increases in phospholipid peroxidation or TUNEL-positive cells, suggesting that antioxidant systems were protecting the cardiomyocytes from damage. Many selenoprotein mRNAs were induced by T3- and ISO-treatment, with levels of methionine sulfoxide reductase 1 (MsrB1, also called SelR) mRNA showing the largest increases. MsrB enzymatic activity was also elevated in both models of cardiac stress, while glutathione peroxidase (GPx) activity and thioredoxin reductase (Trxrd) activity were moderately and nonsignificantly increased, respectively. Western blot assays revealed a marked increase in MsrB1 and moderate increases in GPx3, GPx4, and Trxrd1, particularly in T3-treated hearts. Thus, the main response of the selenoproteome during hypertrophy does not involve increased GPx1, but increased GPx3 for reducing extracellular H(2)O(2) and increased GPx4, Trxrd1, and MsrB1 for minimizing intracellular oxidative damage.
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Registered trials
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