ReviewOxidative medicine and cellular longevity2014
The emerging role of TRα1 in cardiac repair: potential therapeutic implications.
Review in Oxidative medicine and cellular longevity, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 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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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
16 citing papers in PubMed, 30 citations in OpenAlex.
- Lipid Hormones at the Intersection of Metabolic Imbalances and Endocrine Disorders.Current issues in molecular biology · 2025Review
- Triiodothyronine protects infarcted myocardium by reducing apoptosis and preserving mitochondria.Basic research in cardiology · 2025Article
- Thyroid Hormone and Heart Failure: Charting Known Pathways for Cardiac Repair/Regeneration.Biomedicines · 2023Review
- Vitamin D, Thyroid Hormones and Cardiovascular Risk: Exploring the Components of This Novel Disease Triangle.Frontiers in physiology · 2021Review
- Thyroid Hormone Signalling Alteration in Diabetic Nephropathy and Cardiomyopathy: a "Switch" to the Foetal Gene Programme.Current diabetes reports · 2020Review
- FoxO1-Dio2 signaling axis governs cardiomyocyte thyroid hormone metabolism and hypertrophic growth.Nature communications · 2020Article
- Thyroid Hormone Signalling: From the Dawn of Life to the Bedside.Journal of molecular evolution · 2020Review
- Diabetic Nephropathy: Novel Molecular Mechanisms and Therapeutic Targets.Frontiers in pharmacology · 2020Review
- The impact of thyroid hormone dysfunction on ischemic heart disease.Endocrine connections · 2019Review
- Thyroid hormone receptor α1 as a novel therapeutic target for tissue repair.Annals of translational medicine · 2018Review
- Modified Low-Dose Triiodo-L-thyronine Therapy Safely Improves Function Following Myocardial Ischemia-Reperfusion Injury.Frontiers in physiology · 2017Article
- Anacardic acid and thyroid hormone enhance cardiomyocytes production from undifferentiated mouse ES cells along functionally distinct pathways.Endocrine · 2016Article
- Cardioprotection and thyroid hormones.Heart failure reviews · 2016Review
- Relationship between left ventricular mechanics and low free triiodothyronine levels after myocardial infarction: a prospective study.Internal and emergency medicine · 2016Article
- Translating thyroid hormone effects into clinical practice: the relevance of thyroid hormone receptor α1 in cardiac repair.Heart failure reviews · 2015Review
- Coronary Microvascular Function and Beyond: The Crosstalk between Hormones, Cytokines, and Neurotransmitters.International journal of endocrinology · 2015Review
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Thyroid hormone (TH) is critical for adapting living organisms to environmental stress. Plasma circulating tri-iodothyronine (T3) levels drop in most disease states and are associated with increased oxidative stress. In this context, T3 levels in plasma appear to be an independent determinant for the recovery of cardiac function after myocardial infarction in patients. Thyroid hormone receptor α1 (TRα1) seems to be crucial in this response; TRα1 accumulates to cell nucleus upon activation of stress induced growth kinase signaling. Furthermore, overexpression of nuclear TRα1 in cardiomyocytes can result in pathological or physiological growth (dual action) in absence or presence of its ligand, respectively. Accordingly, inactivation of TRα1 receptor prevents reactive hypertrophy after myocardial infarction and results in heart failure with increased phospholamban (PLB) expression and marked activation of p38MAPK. In line with this evidence, TH is shown to limit ischemia/reperfusion injury and convert pathologic to physiologic growth after myocardial infarction via TRα1 receptor. TRα1 receptor may prove to be a novel pharmacological target for cardiac repair/regeneration therapies.
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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.