ArticleMolecular medicine (Cambridge, Mass.)2014
Low-dose T₃ replacement restores depressed cardiac T₃ levels, preserves coronary microvasculature and attenuates cardiac dysfunction in experimental diabetes mellitus.
Article in Molecular medicine (Cambridge, Mass.), 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 62 citations in OpenAlex.
- Cardiovascular Risk Determinants in Euthyroid Patients with Obesity: The Strange Case of TSH in Primary Prevention.Journal of clinical medicine · 2026Article
- Effect of Short-Term and Long-Term Non-Physiological T3 Concentrations on Cardiac Stromal Cells: From Cellular Response to In Vivo Adaptation.Medical sciences (Basel, Switzerland) · 2026Article
- Disrupted thyroid hormone-mitochondrial coupling in diabetic cardiomyopathy: a candidate upstream amplifier of metabolic and redox maladaptation.Frontiers in endocrinology · 2026Review
- Rethinking strategies for solving thyroid dysfunction at the heart of cardiovascular disease.Molecular medicine (Cambridge, Mass.) · 2025Review
- Noncoding and coding mechanisms of aging-related heart failure with preserved ejection fraction associated with thyroid dysfunction.Disease models & mechanisms · 2025Article
- Predicting major cardiac and cerebrovascular events in acute coronary syndrome patients using the thyroid hormone sensitivity index.Frontiers in endocrinology · 2025Article
- Nanoscale organization of cardiac calcium channels is dependent on thyroid hormone status.American journal of physiology. Heart and circulatory physiology · 2024Article
- Update on clinical and experimental management of diabetic cardiomyopathy: addressing current and future therapy.Frontiers in endocrinology · 2024Review
- Novel Transcriptomic Interactomes of Noncoding RNAs in the Heart under Altered Thyroid Hormonal States.International journal of molecular sciences · 2023Article
- Article
- Selenium and Selenoproteins at the Intersection of Type 2 Diabetes and Thyroid Pathophysiology.Antioxidants (Basel, Switzerland) · 2022Review
- Role of miR-133/Dio3 Axis in the T3-Dependent Modulation of Cardiac mitoK-ATP Expression.International journal of molecular sciences · 2022Article
- BNP as a New Biomarker of Cardiac Thyroid Hormone Function.Frontiers in physiology · 2020Article
- Adverse transverse-tubule remodeling in a rat model of heart failure is attenuated with low-dose triiodothyronine treatment.Molecular medicine (Cambridge, Mass.) · 2019Article
- Novel uses of thyroid hormones in cardiovascular conditions.Endocrine · 2019Review
- Cardioprotection and Thyroid Hormones in the Clinical Setting of Heart Failure.Frontiers in endocrinology · 2019Review
- Hormone treatments in congestive heart failure.The Journal of international medical research · 2018Review
- Comparison of Therapeutic Triiodothyronine Versus Metoprolol in the Treatment of Myocardial Infarction in Rats.Thyroid : official journal of the American Thyroid Association · 2018Article
- Cardiac Thyroid Hormone Metabolism and Heart Failure.European thyroid journal · 2017Review
- Modified Low-Dose Triiodo-L-thyronine Therapy Safely Improves Function Following Myocardial Ischemia-Reperfusion Injury.Frontiers in physiology · 2017Article
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Authors and funding
10 authors at 4 institutions in 2 countries.
Funding
Abstract
Thyroid dysfunction is common in individuals with diabetes mellitus (DM) and may contribute to the associated cardiac dysfunction. However, little is known about the extent and pathophysiological consequences of low thyroid conditions on the heart in DM. DM was induced in adult female Sprague Dawley (SD) rats by injection of nicotinamide (N; 200 mg/kg) followed by streptozotocin (STZ; 65 mg/kg). One month after STZ/N, rats were randomized to the following groups (N = 10/group): STZ/N or STZ/N + 0.03 μg/mL T3; age-matched vehicle-treated rats served as nondiabetic controls (C). After 2 months of T3 treatment (3 months post-DM induction), left ventricular (LV) function was assessed by echocardiography and LV pressure measurements. Despite normal serum thyroid hormone (TH) levels, STZ/N treatment resulted in reductions in myocardial tissue content of THs (T3 and T4: 39% and 17% reduction versus C, respectively). Tissue hypothyroidism in the DM hearts was associated with increased DIO3 deiodinase (which converts THs to inactive metabolites) altered TH transporter expression, reexpression of the fetal gene phenotype, reduced arteriolar resistance vessel density, and diminished cardiac function. Low-dose T3 replacement largely restored cardiac tissue TH levels (T3 and T4: 43% and 10% increase versus STZ/N, respectively), improved cardiac function, reversed fetal gene expression and preserved the arteriolar resistance vessel network without causing overt symptoms of hyperthyroidism. We conclude that cardiac dysfunction in chronic DM may be associated with tissue hypothyroidism despite normal serum TH levels. Low-dose T3 replacement appears to be a safe and effective adjunct therapy to attenuate and/or reverse cardiac remodeling and dysfunction induced by experimental DM.
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