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Cardioprotection and thyroid hormones

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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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Abbreviations

HF:

Heart failure

CV:

Cardiovascular

TH:

Thyroid hormone

ATP:

Adenosine triphosphate

H+ :

Hydrogen ions

PKC:

Protein kinase C

ERK:

Extracellular signal-regulated kinases

AKT:

Protein kinase B

ROS:

Reactive oxygen species

I/R:

Ischemic/reperfusion

BCL-2:

B cell lymphoma-2

PTP:

Permeability transition pore

PTPO:

Opening of the PTP

L-T3S:

Low T3 syndrome

AMI:

Acute myocardial infarction

T3:

Triiodothyronine

rT3:

Reverse T3

TRs:

TH-specific receptors

p38MAPK:

p38 mitogen-activated protein kinases

HSP:

Heat-shock protein

p53:

Tumor suppressor protein

PI3K:

Phosphoinositide 3-kinase

T4:

Tiroxine

MMPs:

Metalloproteinases

TIMPs:

Tissue inhibitors of MMPs

TGF:

Transforming growth factor

bFGF:

Fibroblastic growth factor

VEGF:

Vascular endothelial growth factor

HIF-1α:

Hypoxia-inducible factor 1 alpha

mTOR:

Mammalian target of rapamycin

MHC:

Myosin heavy chain

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Correspondence to Alessandro Pingitore.

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The authors of the paper “Cardioprotection and Thyroid Hormones,” Alessandro Pingitore, Giuseppina Nicolini, Claudia Kusmic, Giorgio Iervasi, Paolo Grigolini and Simona Forini declare that they have no conflict of interest.

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Pingitore, A., Nicolini, G., Kusmic, C. et al. Cardioprotection and thyroid hormones. Heart Fail Rev 21, 391–399 (2016). https://doi.org/10.1007/s10741-016-9545-8

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