ReviewVascular pharmacology
Signaling mechanisms in thyroid hormone-induced cardiac hypertrophy.
Review in Vascular pharmacology. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers, 1 of them a synthesis that pooled it.
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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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Who cites it
20 citing papers in PubMed, 1 synthesis or guideline pooled it, 76 citations in OpenAlex.
- The Value of Decreased Thyroid Hormone for Predicting Mortality in Adult Septic Patients: A Systematic Review and Meta-Analysis.Scientific reports · 2018Pooled it
- 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
- Rethinking strategies for solving thyroid dysfunction at the heart of cardiovascular disease.Molecular medicine (Cambridge, Mass.) · 2025Review
- Prognostic significance of FT3 levels in hypertrophic cardiomyopathy patients with HFpEF.Frontiers in cardiovascular medicine · 2025Article
- Cardioprotective effect of Vitamin D on cardiac hypertrophy through improvement of mitophagy and apoptosis in an experimental rat model of levothyroxine -induced hyperthyroidism.Molecular biology reports · 2024Article
- Regression of cardiac hypertrophy in health and disease: mechanisms and therapeutic potential.Nature reviews. Cardiology · 2023Review
- Thyroid hormone-dependent oligodendroglial cell lineage genomic and non-genomic signaling through integrin receptors.Frontiers in pharmacology · 2022Review
- Left ventricular phosphorylation patterns of Akt and ERK1/2 after triiodothyronine intracoronary perfusion in isolated hearts and short-termIranian journal of basic medical sciences · 2020Article
- miRNAs that Induce Human Cardiomyocyte Proliferation Converge on the Hippo Pathway.Cell reports · 2018Article
- microRNA and thyroid hormone signaling in cardiac and skeletal muscle.Cell & bioscience · 2017Review
- Cardiac ACE2/angiotensin 1-7/Mas receptor axis is activated in thyroid hormone-induced cardiac hypertrophy.Therapeutic advances in cardiovascular disease · 2016Article
- MuRF1 mono-ubiquitinates TRα to inhibit T3-induced cardiac hypertrophy in vivo.Journal of molecular endocrinology · 2016Article
- Type 2 Iodothyronine Deiodinase Activity Is Required for Rapid Stimulation of PI3K by Thyroxine in Human Umbilical Vein Endothelial Cells.Endocrinology · 2015Article
- Hypertrophic response of the association of thyroid hormone and exercise in the heart of rats.Arquivos brasileiros de cardiologia · 2014Article
- Thyroid Hormone-Regulated Cardiac microRNAs are Predicted to Suppress Pathological Hypertrophic Signaling.Frontiers in endocrinology · 2014Article
- 3,3'-Diindolylmethane protects against cardiac hypertrophy via 5'-adenosine monophosphate-activated protein kinase-α2.PloS one · 2013Article
- Regulation of gene expression with thyroid hormone in rats with myocardial infarction.PloS one · 2012Article
- Article
- Thyroid hormone can favorably remodel the diabetic myocardium after acute myocardial infarction.Molecular and cellular biochemistry · 2010Article
- Triiodothyronine promotes cardiac differentiation and maturation of embryonic stem cells via the classical genomic pathway.Molecular endocrinology (Baltimore, Md.) · 2010Article
Corrections and comments
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Authors and funding
1 author at 1 institution in 1 country.
Funding
Abstract
Cardiac hypertrophy is a significant independent risk factor for increased mortality, comprising of maladaptive changes in cellular, molecular and metabolic processes that ultimately lead to heart failure. However, cardiac hypertrophy represents a continuum from physiological to compensatory to pathological hypertrophy, so that treatment modalities aimed to shift hypertrophy towards the physiological phenotype would represent an attractive therapeutic strategy. Many of the physiological changes caused by thyroid hormone (TH) treatment may provide direct benefit to the failing heart. Recent experimental studies have shown that TH rapidly activates pro-survival PKB/Akt-mTOR signaling pathways, thus providing cytoprotection and increasing synthesis of normal contractile proteins and metabolic enzymes. TH induces a normal physiological phenotype by binding to nuclear TH receptors that regulate expression of specific genes which promote cell survival and enhance contractile function. Physiological cardiac growth occurs with a coordinated angiogenic response that normalizes myocardial perfusion during hypertrophy, and recent studies support a significant role for TH and its endothelial cell surface integrin receptors and nuclear receptors in neovascularization during TH-induced hypertrophy. The present review examines these molecular mechanisms and intracellular signaling pathways activated in thyroid hormone-induced cardiac hypertrophy that support its therapeutic potential in the treatment of heart disease.
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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.