ArticleMolecular and cellular biochemistry2015
T3 and T4 decrease ROS levels and increase endothelial nitric oxide synthase expression in the myocardium of infarcted rats.
Article in Molecular and cellular biochemistry, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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15 citing papers in PubMed, 39 citations in OpenAlex.
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- Evaluation of the use of the myocardial performance index as a parameter of cardiac function in two experimental models of heart disease: myocardial infarction and pulmonary hypertension.Pflugers Archiv : European journal of physiology · 2025Article
- Association between peripheral thyroid sensitivity defined by the FT3/FT4 ratio and composite adverse outcome among inpatients with heart failure.Frontiers in endocrinology · 2025Article
- Nebivolol in oral subacute treatment prevents cardiac post-ischemic dysfunction in rats, but hyperthyroidism reduces this protection: mechanisms involved.Naunyn-Schmiedeberg's archives of pharmacology · 2024Article
- Vascular Response of Triiodothyronine on Isolated Aortic Rings: Contribution of Redox Mechanisms.Arquivos brasileiros de cardiologia · 2024Article
- Pterostilbene Reduces Experimental Myocardial Infarction-Induced Oxidative Stress in Lung and Right Ventricle.Arquivos brasileiros de cardiologia · 2022Article
- Deiodinases and the Three Types of Thyroid Hormone Deiodination Reactions.Endocrinology and metabolism (Seoul, Korea) · 2021Review
- D-Tagatose Feeding Reduces the Risk of Sugar-Induced Exacerbation of Myocardial I/R Injury When Compared to Its Isomer Fructose.Frontiers in molecular biosciences · 2021Article
- Premature synaptic mitochondrial dysfunction in the hippocampus during aging contributes to memory loss.Redox biology · 2020Article
- Protective Effects of Crocetin on Arsenic Trioxide-Induced Hepatic Injury: Involvement of Suppression in Oxidative Stress and Inflammation Through Activation of Nrf2 Signaling Pathway in Rats.Drug design, development and therapy · 2020Article
- Effect of Hypovitaminosis D on Lipid Profile in Hypothyroid Patients in Saudi Arabia.Oxidative medicine and cellular longevity · 2020Article
- Protective Effects of Euthyroidism Restoration on Mitochondria Function and Quality Control in Cardiac Pathophysiology.International journal of molecular sciences · 2019Review
- Association between Low Free Triiodothyronine Levels and Poor Prognosis in Patients with Acute ST-Elevation Myocardial Infarction.BioMed research international · 2018Observational
- Triiodothyronine differentially modulates the LH and FSH synthesis and secretion in male rats.Endocrine · 2018Article
- Secoisolariciresinol diglucoside attenuates cardiac hypertrophy and oxidative stress in monocrotaline-induced right heart dysfunction.Molecular and cellular biochemistry · 2017Article
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Authors and funding
12 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
unlabelledMyocardial infarction leads to a reduction in nitric oxide (NO) bioavailability and an increase in reactive oxygen species (ROS) levels. This scenario has been shown to be detrimental to the heart. Recent studies have shown that thyroid hormone (TH) administration presents positive effects after ischaemic injury. Based on this, the aim of this study was to evaluate the effect of TH on NO bioavailability as well as on endothelial nitric oxide synthase (eNOS) expression after myocardial infarction. Male Wistar rats were divided into three groups: Sham-operated (SHAM), infarcted (AMI) and infarcted + TH (AMIT). During 26 days, the AMIT group received T3 and T4 (2 and 8 µg/100 g/day, respectively) by gavage, while SHAM and AMI rats received saline. After this, the rats underwent echocardiographic analysis were sacrificed, and the left ventricle was collected for biochemical and molecular analysis. STATISTICAL ANALYSIS: one-way ANOVA with Student-Newman-Keuls post test. AMI rats presented a 38% increase in ROS levels. TH administration prevented these alterations in AMIT rats. The AMIT group presented an increase in eNOS expression, in NOS activity and in nitrite levels. TH administration also increased PGC-1α expression in the AMIT group. In conclusion, TH effects seem to involve a modulation of eNOS expression and an improvement in NO bioavailability in the infarcted heart.
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