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Updated: Mar 23, 2026

In vitro Assessment of Myocardial Protection following Hypothermia-Preconditioning in a Human Cardiac Myocytes Model
Published on: October 27, 2020
Cardioprotection and thyroid hormones
Alessandro Pingitore1, Giuseppina Nicolini2, Claudia Kusmic2
1Clinical Physiology Institute, CNR, Via Moruzzi 1, 56124, Pisa, Italy. pingitor@gmail.com.
Insights
Triiodothyronine shows promise in cardioprotection after heart attack by preserving mitochondria and promoting cell regeneration. This thyroid hormone may reduce infarct size and prevent heart failure progression.
Area of Science:
- Cardiology
- Endocrinology
- Molecular Biology
Background:
- Cardiac disease progression post-ischemia involves complex mechanisms including ischemic damage, reperfusion injury, and remodeling.
- Cardioprotection aims to reduce infarct size and prevent heart failure after acute ischemic events.
- Effective cardioprotective strategies require targeting interconnected pathways involved in disease progression.
Purpose of the Study:
- To review the cardioprotective role of triiodothyronine in the context of post-ischemic cardiac disease evolution.
- To highlight how triiodothyronine influences key mechanisms in the heart after ischemia.
Main Methods:
- Literature review focusing on studies investigating the thyroid system and heart homeostasis.
- Analysis of research on triiodothyronine's effects on mitochondrial function, fibrosis, angiogenesis, and cell regeneration in cardiac tissue.
- Synthesis of findings related to triiodothyronine's impact on post-ischemic cardiac remodeling.
Main Results:
- Triiodothyronine plays a significant role in preserving mitochondrial function and morphology.
- It exhibits antifibrotic and proangiogenetic effects, crucial for cardiac repair.
- Potential for triiodothyronine to induce cell regeneration and growth in the post-ischemic heart.
Conclusions:
- Triiodothyronine demonstrates multifaceted cardioprotective effects relevant to post-ischemic cardiac disease.
- Targeting the thyroid system, specifically with triiodothyronine, represents a promising therapeutic avenue for reducing infarct size and mitigating heart failure.
- Further research into triiodothyronine's mechanisms could lead to novel cardioprotective interventions.
Abstract:
The evolution of cardiac disease after an acute ischemic event depends on a complex and dynamic network of mechanisms alternating from ischemic damage due to acute coronary occlusion to reperfusion injury due to the adverse effects of coronary revascularization till post-ischemic remodeling. Cardioprotection is a new purpose of the therapeutic interventions in cardiology with the goal to reduce infarct size and thus prevent the progression toward heart failure after an acute ischemic event. In a complex biological system such as the human one, an effective cardioprotective strategy should diachronically target the network of cross-talking pathways underlying the disease progression. Thyroid system is strictly interconnected with heart homeostasis, and recent studies highlighted its role in cardioprotection, in particular through the preservation of mitochondrial function and morphology, the antifibrotic and proangiogenetic effect and also to the potential induction of cell regeneration and growth. The objective of this review was to highlight the cardioprotective role of triiodothyronine in the complexity of post-ischemic disease evolution.
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