ReviewInternational journal of molecular sciences2020
Genomic and Non-Genomic Mechanisms of Action of Thyroid Hormones and Their Catabolite 3,5-Diiodo-L-Thyronine in Mammals.
Review in International journal of molecular sciences, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.
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Who cites it
41 citing papers in PubMed, 86 citations in OpenAlex.
- RXR Gamma Enables Oligodendrocyte Differentiation by Suppressing Sonic Hedgehog Signaling.Glia · 2026Article
- Navigating thyroid hormone signaling in liver fibrosis: mechanisms and clinical implications.Journal of endocrinological investigation · 2026Review
- Metabolic profiling of steatotic liver disease by fluorescence lifetime imaging microscopy.Communications medicine · 2026Article
- Effects of 3,3',5-triiodothyronine supplementation during ex vivo lung perfusion on ischemia/reperfusion injury in rat lungs.Frontiers in medicine · 2026Article
- Cardiac Endocrine Function and Hormonal Interplay in Pediatrics: From Development to Clinical Implications.Biomedicines · 2025Review
- Nongenomic Stimulatory Effect of T3 on Calcium Dynamics in GnRH Neurons via Integrin αVβ3.Endocrinology · 2025Article
- Nutrition and Micronutrient Interactions in Autoimmune Thyroid Disorders: Implications for Cardiovascular Health.Pathophysiology : the official journal of the International Society for Pathophysiology · 2025Review
- The impact of autoimmune thyroid disease on cognitive and psychiatric disorders: focus on clinical, pre-clinical and molecular studies.European thyroid journal · 2025Review
- Review
- Thyroid hormones inhibit tumor progression and enhance the antitumor activity of lenvatinib in hepatocellular carcinoma via reprogramming glucose metabolism.Cell death discovery · 2025Article
- Review
- Clinical characteristics of Graves' disease following COVID-19 infection or vaccination: a multicenter case-control study.Turkish journal of medical sciences · 2025Article
- Article
- Thyroid hormone suppresses cell growth by regulating CDK2 and cyclin E1 expression via Hepsin.American journal of cancer research · 2025Article
- Thyroid Hormones and Co-workers: An Overview.Methods in molecular biology (Clifton, N.J.) · 2025Review
- Effects and Impact of Selenium on Human Health, A Review.Molecules (Basel, Switzerland) · 2024Review
- The impact of thyroid disorder on cardiovascular disease: Unraveling the connection and implications for patient care.International journal of cardiology. Heart & vasculature · 2024Review
- Sex-Specific Effects of THRβ Signaling on Metabolic Responses to High Fat Diet in Mice.Endocrinology · 2024Article
- Three candidate SNPs show associations with thyroid-stimulating hormone in euthyroid subjects: Tehran thyroid study.Journal of diabetes and metabolic disorders · 2024Article
- The Expression of Neurodegeneration-Related Genes in the Hippocampus of Hypothyroid Rats Following Long-Term Potentiation.The Eurasian journal of medicine · 2024Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Since the realization that the cellular homologs of a gene found in the retrovirus that contributes to erythroblastosis in birds (v-erbA), i.e. the proto-oncogene c-erbA encodes the nuclear receptors for thyroid hormones (THs), most of the interest for THs focalized on their ability to control gene transcription. It was found, indeed, that, by regulating gene expression in many tissues, these hormones could mediate critical events both in development and in adult organisms. Among their effects, much attention was given to their ability to increase energy expenditure, and they were early proposed as anti-obesity drugs. However, their clinical use has been strongly challenged by the concomitant onset of toxic effects, especially on the heart. Notably, it has been clearly demonstrated that, besides their direct action on transcription (genomic effects), THs also have non-genomic effects, mediated by cell membrane and/or mitochondrial binding sites, and sometimes triggered by their endogenous catabolites. Among these latter molecules, 3,5-diiodo-L-thyronine (3,5-T2) has been attracting increasing interest because some of its metabolic effects are similar to those induced by T3, but it seems to be safer. The main target of 3,5-T2 appears to be the mitochondria, and it has been hypothesized that, by acting mainly on mitochondrial function and oxidative stress, 3,5-T2 might prevent and revert tissue damages and hepatic steatosis induced by a hyper-lipid diet, while concomitantly reducing the circulating levels of low density lipoproteins (LDL) and triglycerides. Besides a summary concerning general metabolism of THs, as well as their genomic and non-genomic effects, herein we will discuss resistance to THs and the possible mechanisms of action of 3,5-T2, also in relation to its possible clinical use as a drug.
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