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TH Metabolism in Ischemia/Reperfusion Models

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Thyroid and Heart

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Abstract

Clinical evidence has shown that the two major outcomes of thyroid disease, namely, hypothyroidism and hyperthyroidism, cause evident alterations in haemodynamics and cardiac function. Moreover, even subclinical conditions of thyroid dysfunction represent higher risk for cardiovascular disease (CVD). On the other hand, clinical observations have also highlighted that CVD such as acute infarction and heart failure are associated with reduced T3 state, even in the absence of overt thyroid disorders in about 15–30% of cases. For a long time, the hypothesis underlying these observations has been that peripheral reduction of T4 conversion to T3 or inactivation to rT3 could be an adaptive response of myocardial tissue to reduce metabolic demands under stressful conditions. However, clinical evidence has proven that a persistent low T3 condition may have adverse cardiac prognostic outcomes. Moreover, a few clinical trials have shown that the replacement of homeostatic doses of thyroid hormones have a positive role in ameliorating the severity of CVD. These findings paved the way to explore new therapeutic strategies in the field of CVD and to investigate the cellular and molecular basis of such potential cardioprotective effects of thyroid hormones through experimental studies. The examination of individual cell pathways and more complex high-throughput analyses have currently provided a broader picture of T3 action during acute infarction and in the postischemic setting. It includes genomic and non-genomic mechanisms of action and crosstalk between T3 and specific miRNAs for the post-translational regulation of a wide range of genes involved in many cellular processes. Mitochondria, whose cellular functions are pleiotropic and go well beyond the mere regulation of bioenergetics, have also emerged as a pivotal target of T3 action.

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  1. Institute of Clinical Physiology, CNR, Pisa, Italy

    Claudia Kusmic & Serena L’Abbate

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  1. Claudia Kusmic
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  2. Serena L’Abbate
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Correspondence to Claudia Kusmic .

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Editors and Affiliations

  1. Institute of Clinical Physiology (IFC) National Research Council (CNR), Pisa, Italy

    Giorgio Iervasi

  2. Institute of Clinical Physiology (IFC) National Research Council (CNR), Pisa, Italy

    Alessandro Pingitore

  3. NYITCOM College of Osteopathic Medicine Biomedical Sciences Department, Old Westbury, NY, USA

    A.Martin Gerdes

  4. Institute of Clinical and Translational Medicine, Newcastle University/Queen Elizabeth Hospital, Newcastle upon Tyne, UK

    Salman Razvi

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Kusmic, C., L’Abbate, S. (2020). TH Metabolism in Ischemia/Reperfusion Models. In: Iervasi, G., Pingitore, A., Gerdes, A., Razvi, S. (eds) Thyroid and Heart . Springer, Cham. https://doi.org/10.1007/978-3-030-36871-5_6

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