ArticleMolecular and cellular biochemistry2011
Acute T3 treatment protects the heart against ischemia-reperfusion injury via TRα1 receptor.
Article in Molecular and cellular biochemistry, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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Who cites it
29 citing papers in PubMed, 51 citations in OpenAlex.
- Cardioprotective therapies for ST-elevation myocardial infarction: the emerging role of thyroid hormone: a narrative review.Frontiers in endocrinology · 2025Review
- Nebivolol in oral subacute treatment prevents cardiac post-ischemic dysfunction in rats, but hyperthyroidism reduces this protection: mechanisms involved.Naunyn-Schmiedeberg's archives of pharmacology · 2024Article
- Donor Heart Preservation: Current Knowledge and the New Era of Machine Perfusion.International journal of molecular sciences · 2023Review
- Synergistic effects of hormones on structural and functional maturation of cardiomyocytes and implications for heart regeneration.Cellular and molecular life sciences : CMLS · 2023Review
- Adrenal response to ACTH challenge alters thyroid and immune function and varies with body reserves in molting adult female northern elephant seals.American journal of physiology. Regulatory, integrative and comparative physiology · 2023Article
- Nrf2-Mediated Antioxidant Defense and Thyroid Hormone Signaling: A Focus on Cardioprotective Effects.Antioxidants (Basel, Switzerland) · 2023Review
- Cardioprotection by Hypothyroidism Is Not Mediated by Favorable Hemodynamics-Role of Canonical Thyroid Hormone Receptor Alpha Signaling.International journal of molecular sciences · 2022Article
- The Potential of Thyroid Hormone Therapy in Severe COVID-19: Rationale and Preliminary Evidence.International journal of environmental research and public health · 2022Review
- Effects of Thyroid Hormone on Tissue Hypoxia: Relevance to Sepsis Therapy.Journal of clinical medicine · 2021Review
- Cardioprotective effects of triiodothyronine supplementation against ischemia reperfusion injury by preserving calcium cycling proteins in isolated rat hearts.Experimental and therapeutic medicine · 2019Article
- 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
- Cardioprotective effect of thyroid hormone is mediated by AT2 receptor and involves nitric oxide production via Akt activation in mice.Heart and vessels · 2018Article
- Similarities and Differences in the Peripheral Actions of Thyroid Hormones and Their Metabolites.Frontiers in endocrinology · 2018Review
- Cardiac ischemia/reperfusion injury is inversely affected by thyroid hormones excess or deficiency in male Wistar rats.PloS one · 2018Article
- Relation of Low T3 to One-Year Mortality in Non-ST-Elevation Acute Coronary Syndrome Patients.Journal of clinical laboratory analysis · 2017Article
- Altered thyroid status affects myocardial expression of connexin-43 and susceptibility of rat heart to malignant arrhythmias that can be partially normalized by red palm oil intake.Histochemistry and cell biology · 2017Article
- Role of the Thyroid System in the Dynamic Complex Network of Cardioprotection.European cardiology · 2016Review
- Cardioprotection and thyroid hormones.Heart failure reviews · 2016Review
- MuRF1 mono-ubiquitinates TRα to inhibit T3-induced cardiac hypertrophy in vivo.Journal of molecular endocrinology · 2016Article
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
We have previously shown that acute thyroid hormone treatment could limit reperfusion injury and increase post-ischemic recovery of function. In the present study, we further explore potential initiating mechanisms of this response. Thus, isolated rat hearts were subjected to 30 min zero-flow global ischemia (I) followed by 60-min reperfusion (R). Reperfusion injury was assessed by post-ischemic recovery of left ventricular developed pressure (LVDP%) and LDH release. T3 at a dose of 60 nM which had no effect on contractile function of non-ischemic myocardium, significantly increased LVDP% [48% (2.9) vs. 30.2% (3.3) for untreated group, P < 0.05] and reduced LDH release [8.3 (0.3) vs. 10 (0.42) for untreated group, P < 0.05] when administered at R. T4 (60 and 400 nM) had no effect on contractile function either in non-ischemic or ischemic myocardium. Administration of debutyl-dronedarone (DBD), a TRα1 antagonist abolished the T3-limiting effect on reperfusion injury: Thus, co-administration of T3 and DBD resulted in significantly lower LVDP%, [23% (4.7) vs. 48% (2.9) for T3 group, P < 0.05] and higher LDH release [9.9 (0.3) vs. 8.3 (0.3), for T3 group, P < 0.05]. In conclusion, acute T3 and not T4 treatment will be able to protect against reperfusion injury. T3 can exert this beneficial effect on ischemic myocardium at a dose that has no effects on non-ischemic myocardium. Acute T3-limiting effect on reperfusion injury is mediated, at least in part, via TRα1 receptor.
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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.