ArticleCardiovascular research2010
Thyroid hormone stimulates NO production via activation of the PI3K/Akt pathway in vascular myocytes.
Article in Cardiovascular research, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 71 papers, 1 of them a synthesis that pooled it.
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Who cites it
71 citing papers in PubMed, 1 synthesis or guideline pooled it, 156 citations in OpenAlex.
- American Thyroid Association Guide to investigating thyroid hormone economy and action in rodent and cell models.Thyroid : official journal of the American Thyroid Association · 2014Guideline
- Asymmetric U-shaped association between first-trimester maternal free thyroxine levels and the risk of preeclampsia: a large-scale cohort study.Journal of hypertension · 2026Article
- Free triiodothyronine in intracranial aneurysms: a sex-specific association with unruptured disease and a non-thyroidal illness signal after rupture.Frontiers in neurology · 2026Article
- Molecular Drivers of Vascular Adaptation in Young Athletes: An Integrative Analysis of Endothelial, Metabolic and Lipoprotein Biomarkers.Biomolecules · 2025Article
- The Role of Thyroid Hormones in Neurodegenerative Disorders: Opportunities and Challenges.Molecular neurobiology · 2025Review
- Hypothyroidism in spontaneous coronary artery dissection: presentation, clinical and angiographic findings, management and outcomes.Open heart · 2025Article
- Article
- Thyroxine Treatment after Traumatic Brain Injury Suppresses Astrogliosis and Enhances Neuronal Recovery in Mice.Thyroid : official journal of the American Thyroid Association · 2025Article
- Associations of Thyroid and Parathyroid Hormones with Arterial Stiffness in Emergency Department Patients: A Prospective Cross-Sectional Study.Medicina (Kaunas, Lithuania) · 2025Article
- L-Arginine and Nitric Oxide in Vascular Regulation-Experimental Findings in the Context of Blood Donation.Nutrients · 2025Review
- Investigation of the mechanism of hypertension caused by BTKi in the treatment of hematologic diseases.Frontiers in pharmacology · 2025Review
- Cardiovascular Findings and Effects of Caffeine on Experimental Hypothyroidism.Endocrine, metabolic & immune disorders drug targets · 2025Article
- Metabolic Syndrome, Thyroid Dysfunction, and Cardiovascular Risk: The Triptych of Evil.International journal of molecular sciences · 2024Review
- Article
- Hypothyroidism and metabolic cardiovascular disease.Frontiers in endocrinology · 2024Review
- Circulating thyroid hormones and clinical parameters of heart failure in men.Scientific reports · 2023Article
- Triiodothyronine and Protein Malnutrition Could Influence Pulse Wave Velocity in Pre-Dialysis Chronic Kidney Disease Patients.Diagnostics (Basel, Switzerland) · 2023Article
- Analysis of Risk Factors for Major Adverse Cardiovascular Events in Patients with Coronary Stent Restenosis after Revascularization.Reviews in cardiovascular medicine · 2023Article
- Transiently impaired endothelial function during thyroid hormone withdrawal in differentiated thyroid cancer patients.Frontiers in endocrinology · 2023Article
- Arterial Stiffness in Thyroid and Parathyroid Disease: A Review of Clinical Studies.Journal of clinical medicine · 2022Review
11 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 2 institutions in 3 countries.
Funding
Abstract
aimsThyroid hormone (TH) rapidly relaxes vascular smooth muscle cells (VSMCs). However, the mechanisms involved in this effect remain unclear. We hypothesize that TH-induced rapid vascular relaxation is mediated by VSMC-derived nitric oxide (NO) production and is associated with the phosphatidylinositol 3-kinase/protein kinase B (PI3K/Akt) signalling pathway. METHODS AND
resultsNO levels were determined using a NO-specific fluorescent dye (DAF-2) and nitrite (NO2-) levels. Expression of NO synthase (NOS) isoforms and proteins of the PI3K/Akt pathway was determined by both western blotting and immunocytochemistry. Myosin light chain (MLC) phosphorylation levels were also investigated by western blotting. Exposure of cultured VSMCs from rat thoracic aortas to triiodothyronine (T3) resulted in a significant decrease of MLC phosphorylation levels. T3 also induced a rapid increase in Akt phosphorylation and increased NO production in a dose-dependent manner (0.001-1 microM). VSMCs stimulated with T3 for 30 min showed an increase in the expression of all three NOS isoforms and augmented NO production, effects that were prevented by inhibitors of PI3K. Vascular reactivity studies showed that vessels treated with T3 displayed a decreased response to phenylephrine, which was reversed by NOS inhibition. These data suggest that T3 treatment induces greater generation of NO both in aorta and VSMCs and that this phenomenon is endothelium independent. In addition, these findings show for the first time that the PI3K/Akt signalling pathway is involved in T3-induced NO production by VSMCs, which occurs with expressive participation of inducible and neuronal NOS.
conclusionOur data strongly indicate that T3 causes NO-dependent rapid relaxation of VSMC and that this effect is mediated by the PI3K/Akt signalling pathway.
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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.