ArticlePloS one2018
Cardiac ischemia/reperfusion injury is inversely affected by thyroid hormones excess or deficiency in male Wistar rats.
Article in PloS one, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 27 citations in OpenAlex.
- 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
- Effect of Cold Adaptation on the State of Cardiovascular System and Cardiac Tolerance to Ischemia/Reperfusion Injury.Iranian biomedical journal · 2024Review
- The predictive value of the nomogram model of clinical risk factors for ischemia-reperfusion injury after primary percutaneous coronary intervention.Scientific reports · 2023Article
- Cardioprotection by Hypothyroidism Is Not Mediated by Favorable Hemodynamics-Role of Canonical Thyroid Hormone Receptor Alpha Signaling.International journal of molecular sciences · 2022Article
- Effect of Radioimmunoassay on Accuracy of Thyroid Hormone Detection.Contrast media & molecular imaging · 2022Article
- Oxidative Stress in the Protection and Injury of the Lacrimal Gland and the Ocular Surface: are There Perspectives for Therapeutics?Frontiers in cell and developmental biology · 2022Review
- Targeted Mitochondrial Drugs for Treatment of Ischemia-Reperfusion Injury.Current drug targets · 2022Review
- Zenglv Fumai Granule protects cardiomyocytes against hypoxia/reoxygenation-induced apoptosis via inhibiting TRIM28 expression.Molecular medicine reports · 2021Article
- Improving translational research in sex-specific effects of comorbidities and risk factors in ischaemic heart disease and cardioprotection: position paper and recommendations of the ESC Working Group on Cellular Biology of the Heart.Cardiovascular research · 2021Review
- The co-treatment of rosuvastatin with dapagliflozin synergistically inhibited apoptosis via activating the PI3K/AKt/mTOR signaling pathway in myocardial ischemia/reperfusion injury rats.Open medicine (Warsaw, Poland) · 2021Article
- Dynorphins in Development and Disease: Implications for Cardiovascular Disease.Current molecular medicine · 2020Review
- Changes in the Stoichiometry of Uniplex Decrease Mitochondrial Calcium Overload and Contribute to Tolerance of Cardiac Ischemia/Reperfusion Injury in Hypothyroidism.Thyroid : official journal of the American Thyroid Association · 2019Article
- Selenium-Rich Diet Induces Myocardial Structural and Functional Abnormalities by Activating Caspase-9 and Caspase-3 in Gpx-1P198L-Overexpression Transgenic Mice.Medical science monitor : international medical journal of experimental and clinical research · 2019Article
- Propranolol inhibits myocardial infarction-induced brown adipose tissue D2 activation and maintains a low thyroid hormone state in rats.Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologica · 2019Article
- Neurological and Inflammatory Manifestations in Sjögren's Syndrome: The Role of the Kynurenine Metabolic Pathway.International journal of molecular sciences · 2018Review
- Berberine inhibits cardiac remodeling of heart failure after myocardial infarction by reducing myocardial cell apoptosis in rats.Experimental and therapeutic medicine · 2018Article
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
aimThyroid dysfunctions can increase the risk of myocardial ischemia and infarction. However, the repercussions on cardiac ischemia/reperfusion (IR) injury remain unclear so far. We report here the effects of hypothyroidism and thyrotoxicosis in the susceptibility to IR injury in isolated rat hearts compared to euthyroid condition and the potential role of antioxidant enzymes.
methodsHypothyroidism and thyrotoxicosis were induced by administration of methimazole (MMZ, 300 mg/L) and thyroxine (T4, 12 mg/L), respectively in drinking water for 35 days. Isolated hearts were submitted to IR and evaluated for mechanical dysfunctions and infarct size. Superoxide dismutase types 1 and 2 (SOD1 and SOD2), glutathione peroxidase types 1 and 3 (GPX 1 and GPX3) and catalase mRNA levels were assessed by quantitative RT-PCR to investigate the potential role of antioxidant enzymes.
resultsThyrotoxicosis elicited cardiac hypertrophy and increased baseline mechanical performance, including increased left ventricle (LV) systolic pressure, LV developed pressure and derivatives of pressure (dP/dt), whereas in hypothyroid hearts exhibited decreased dP/dt. Post-ischemic recovery of LV end-diastolic pressure (LVEDP), LVDP and dP/dt was impaired in thyrotoxic rat hearts, whereas hypothyroid hearts exhibited improved LVEDP and decreased infarct size. Catalase expression was decreased by thyrotoxicosis.
conclusionThyrotoxicosis was correlated, at least in part, to cardiac remodeling and increased susceptibility to IR injury possibly due to down-regulation of antioxidant enzymes, whereas hypothyroid hearts were less vulnerable to IR injury.
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