Impact of hyperthyroidism on cardiac hypertrophy

Barreto‐Chaves, Maria Luíza Morais; Senger, Nathalia; Fevereiro, Marina; Parletta, Aline Cristina; Takano, Ana Paula Cremasco

doi:10.1530/ec-19-0543

Cited by 28 publications

(19 citation statements)

References 122 publications

(140 reference statements)

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“…In spite of their wide effects on metabolism, the use of THs for therapeutic purposes remains controversial because, as mentioned, these hormones may induce other non-metabolic effects. In more detail, like hyperthyroidism, treatment with exogenous THs can induce thyrotoxicosis, a condition characterized by a variety of adverse symptoms, such weight loss, osteoporosis, atrial fibrillation, embolic events, and increased risk of heart failure [33,34,181].…”

Section: The 35-diodothyronine (35-t2) As a Hormonementioning

confidence: 99%

“…Given their action on metabolism, it seemed, in the past, that they could be used as pharmacological agents for the treatment of obesity. However, this approach could be not applied, due to adverse side effects on many organs and systems and, in particular, on the cardiovascular system and the heart's rhythm [33,34]. Yet, in recent years, it has been found that some metabolites of thyroid hormones, and especially 3,5-diiodo-L-thyronine (3,5-T2), are endowed with interesting metabolic activities that may be of clinical interest as possible therapeutic options in the treatment of overeating disorders [20].…”

Section: Introductionmentioning

confidence: 99%

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Genomic and Non-Genomic Mechanisms of Action of Thyroid Hormones and Their Catabolite 3,5-Diiodo-L-Thyronine in Mammals

Giammanco

Schiera

Liegro

2020

IJMS

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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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Section: The 35-diodothyronine (35-t2) As a Hormonementioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Genomic and Non-Genomic Mechanisms of Action of Thyroid Hormones and Their Catabolite 3,5-Diiodo-L-Thyronine in Mammals

Giammanco

Schiera

Liegro

2020

IJMS

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“…D3, with substrate affinity T4>T3 and function for T3 degradation, is similar in activity to D1_2 and found in the central nervous system. From its localization at the plasma membrane D3 may migrate to the nuclear membrane in ischemia, where it inactivates T4 and T3 ( 26 ).…”

Section: Blood Transport Metabolisation Cellular Uptake and Cellular Effects Of Thmentioning

confidence: 99%

Physiological Role and Use of Thyroid Hormone Metabolites - Potential Utility in COVID-19 Patients

Frőhlich

Wahl

2021

Front. Endocrinol.

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Thyroxine and triiodothyronine (T3) are classical thyroid hormones and with relatively well-understood actions. In contrast, the physiological role of thyroid hormone metabolites, also circulating in the blood, is less well characterized. These molecules, namely, reverse triiodothyronine, 3,5-diiodothyronine, 3-iodothyronamine, tetraiodoacetic acid and triiodoacetic acid, mediate both agonistic (thyromimetic) and antagonistic actions additional to the effects of the classical thyroid hormones. Here, we provide an overview of the main factors influencing thyroid hormone action, and then go on to describe the main effects of the metabolites and their potential use in medicine. One section addresses thyroid hormone levels in corona virus disease 19 (COVID-19). It appears that i) the more potently-acting molecules T3 and triiodoacetic acid have shorter half-lives than the less potent antagonists 3-iodothyronamine and tetraiodoacetic acid; ii) reverse T3 and 3,5-diiodothyronine may serve as indicators for metabolic dysregulation and disease, and iii) Nanotetrac may be a promising candidate for treating cancer, and resmetirom and VK2809 for steatohepatitis. Further, the use of L-T3 in the treatment of severely ill COVID-19 patients is critically discussed.

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“…The cardiac renin–angiotensin–aldosterone system (RAAS) has been reported to be activated in hyperthyroidism and that could escalate cardiac renin function and angiotensin II (Ang II) levels [ 42 ]. Besides, the cardiac angiotensin II receptor type 2 (AT2 receptor) was shown to be upregulated in response to hyperthyroidism, suggesting that there are alterations of key molecules of the major axis of RAAS in hyperthyroidism.…”

Section: Introductionmentioning

confidence: 99%

“…Besides, the cardiac angiotensin II receptor type 2 (AT2 receptor) was shown to be upregulated in response to hyperthyroidism, suggesting that there are alterations of key molecules of the major axis of RAAS in hyperthyroidism. Use of angiotensin-converting enzyme (ACE) or angiotensin II receptor type 1 (AT1 receptor) inhibitory drugs were shown to depreciate RAAS in cardiac cell proliferation due to enhanced thyroid hormone and suggest that RAAS acts a pivotal part in thyroid hormone-mediated cardiac hypertrophy [ 42 ].…”

Section: Introductionmentioning

confidence: 99%

SARS-CoV-2 plays a pivotal role in inducing hyperthyroidism of Graves’ disease

Murugan

Alzahrani

2021

Endocrine

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Coronavirus disease 2019 (COVID-19) advances to affect every part of the globe and remains a challenge to the human race. Severe acute respiratory syndrome-coronavirus-2 (SARS-CoV-2) was shown to affect many organs and organ systems including the thyroid gland as these parts highly express angiotensin-converting enzyme 2 (ACE2) protein, which functions as a receptor for initially entering the virus into the cells. Furthermore, some categories of the population including older people and persons with comorbidities are prone to be more vulnerable to COVID-19 and its complications. Recent reports showed that SARS-CoV-2 infection could cause Graves’ disease (autoimmune hyperthyroidism) in post-COVID-19 patients. Factors that may boost the mortality risk of COVID-19 patients are not completely known yet and a clear perception of the group of vulnerable people is also essential. This review briefly summarizes the features of Graves’ disease such as symptoms, risk factors, including environmental, genetic, immunological, and other factors, associated disorders, and therapeutic options. It comprehensively describes the recent advances in SARS-CoV-2-induced Graves’ disease and the pivotal role of autoimmune factors in inducing the disease. The review also discusses the possible risks of SARS-CoV-2 infection and associated COVID-19 in people with hyperthyroidism. Furthermore, it explains thyroid disease and its association with the severity of COVID-19.

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Impact of hyperthyroidism on cardiac hypertrophy

Cited by 28 publications

References 122 publications

Genomic and Non-Genomic Mechanisms of Action of Thyroid Hormones and Their Catabolite 3,5-Diiodo-L-Thyronine in Mammals

Genomic and Non-Genomic Mechanisms of Action of Thyroid Hormones and Their Catabolite 3,5-Diiodo-L-Thyronine in Mammals

Physiological Role and Use of Thyroid Hormone Metabolites - Potential Utility in COVID-19 Patients

SARS-CoV-2 plays a pivotal role in inducing hyperthyroidism of Graves’ disease

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