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Cardioprotection and Thyroid Hormones in the Clinical Setting of Heart Failure
Francesca Mastorci1, Laura Sabatino1, Cristina Vassalle2
1Clinical Physiology Institute, CNR, Pisa, Italy.
Insights
Thyroid hormone (TH) offers cardioprotection against heart failure (HF) by modulating cellular processes and preserving cardiac function. Clinical evidence suggests TH as a potential therapeutic strategy for treating HF patients.
Area of Science:
- Cardiology
- Endocrinology
- Molecular Medicine
Background:
- Ischemic heart disease (IHD) is a leading cause of global mortality, exacerbated by aging populations.
- Cardioprotection involves complex mechanisms of myocardial damage repair and protective factor activation.
- Targeting cardioprotective pathways presents a promising therapeutic avenue for post-ischemic heart failure (HF).
Purpose of the Study:
- To review the clinical evidence supporting the role of the thyroid system in heart failure (HF).
- To explore thyroid hormone (TH)-mediated cardioprotection mechanisms relevant to HF treatment.
Main Methods:
- Review of existing clinical evidence on thyroid hormone's role in heart failure.
- Analysis of studies investigating TH's effects on cardiac function, cellular pathways, and homeostasis.
Main Results:
- Thyroid hormone (TH) influences neuroendocrine systems, inflammation, oxidative stress, and intracellular pro-survival pathways.
- TH impacts cardiac angiogenesis, structure, function, and mitochondrial integrity.
- TH exerts both genomic and non-genomic effects crucial for cardiovascular homeostasis.
Conclusions:
- Thyroid hormone (TH) demonstrates significant cardioprotective effects through diverse mechanisms.
- Clinical evidence supports the potential of TH as a therapeutic agent for heart failure (HF).
- Further research into TH-based therapies could offer new treatment options for HF patients.
Abstract:
Ischemic heart disease is the main cause of morbidity and mortality worldwide and is becoming more widespread with population aging. Cardioprotection is a dynamic process characterized by mechanisms related to myocardial damage and activation of protective factors. Targeting these processes could be attractive as a new therapeutic strategy in the evolution of post-ischemic heart failure (HF). In this context, the role of thyroid hormone (TH)-mediated cardioprotection is supported by a number of findings regarding the modulation of neuroendocrine systems, inflammatory and oxidative stress status, pro-survival intracellular pathways, and epigenetic factors, its effects on cardiac angiogenesis, structure, and function and on the preservation of mitochondrial function and morphology, and its beneficial effects on cell growth and redifferentiation. Moreover, the numerous effects of TH on the heart involve genomic mechanisms, which include cardiac differentiation during the perinatal period and non-genomic action, directed toward the maintenance of cardiovascular homeostasis. This evidence suggests that there is an opportunity to treat HF patients with TH. This review is mainly focused on the clinical evidence of the role of the thyroid system in the complex setting of HF.
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