Thyroxine pretreatment increases basal myocardial heat-shock protein 27 expression and accelerates translocation and phosphorylation of this protein upon ischaemia

Pantos, Constantinos; Malliopoulou, Vassiliki; Mourouzis, Iordanis; Karamanoli, Evangelia; Moraitis, Panagiotis; Tzeis, Stylianos; Paizis, Ioannis; Cokkinos, Alexandros D.; Carageorgiou, Haris; Varonos, D.; Cokkinos, Dennis V.

doi:10.1016/j.ejphar.2003.08.030

Cited by 53 publications

(34 citation statements)

References 34 publications

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“…TH can switch pathological to physiological hypertrophy preserving the ellipsoidal shape of left ventricular chamber shown to protect isolated rat hearts against ischemia and reperfusion and neonatal cardiomyocytes from serum starvation [101][102][103][104][105][106][107]. Even the dobutamine detrimental effect on reperfusion injury can be reversed by T4 pretreatment [104]. Interestingly, improvement in post-ischemic functional recovery is observed despite the fact that diastolic dysfunction is markedly exacerbated upon ischemia (ischemic contracture) [103,108].…”

Section: Th Mimics Preconditioning Effectmentioning

confidence: 96%

“…6 Schematic of molecular, structural and functional changes during postischemic cardiac remodeling. TH can switch pathological to physiological hypertrophy preserving the ellipsoidal shape of left ventricular chamber shown to protect isolated rat hearts against ischemia and reperfusion and neonatal cardiomyocytes from serum starvation [101][102][103][104][105][106][107]. Even the dobutamine detrimental effect on reperfusion injury can be reversed by T4 pretreatment [104].…”

Section: Th Mimics Preconditioning Effectmentioning

confidence: 99%

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New insights into the role of thyroid hormone in cardiac remodeling: time to reconsider?

2010

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Chronic ischemia or pressure overload decreases thyroid hormone (TH) signaling and activates the fetal gene program in the heart. While these features are of physiologic importance in the developing heart, their respective roles in the postnatal heart are debated. Administration of TH can prevent the changes of the fetal gene program and rebuild the heart after an "index event" such as ischemia. TH affects cardiac remodeling by limiting reperfusion injury, and, at later states, by inducing distinct changes in cardiac chamber geometry in a time-dependent manner. Furthermore, administration of TH can convert pathologic to physiologic hypertrophy. These effects are the result of favorable cellular remodeling. While preliminary clinical studies provide encouraging results, the potential and efficacy of TH in the treatment of heart disease still await evaluation in large clinical trials.

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Section: Th Mimics Preconditioning Effectmentioning

confidence: 96%

Section: Th Mimics Preconditioning Effectmentioning

confidence: 99%

New insights into the role of thyroid hormone in cardiac remodeling: time to reconsider?

2010

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“…Interestingly, T3 treatment was associated with a decrease in myocyte ischemia-induced apoptosis, through the non-genomic activation of Akt signaling pathway, which has been shown to play a role in regulating cardiomyocyte growth and survival [122]. Another potential mechanism of THinduced cardioprotection is the increased expression of heat shock proteins such as HSP-27 and HSP-70, two redox-regulated molecular chaperones that enhance cell survival under stress [123,124]. This TH effect seems particularly interesting since in patients with left ventricular dysfunction due to non-atherosclerotic cardiac disease, serum levels of heat shock proteins, IL-6 and CRP are elevated and the entity of this elevation is associated with a more severe disease as evidenced by a more depressed myocardial blood flow at rest and during dypiridamole, indicative of microvascular impairment [125].…”

Section: Effects Of Ths On Myocardial Blood Flowmentioning

confidence: 97%

The role of thyroid hormone in the pathophysiology of heart failure: clinical evidence

2008

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Thyroid hormone (TH) has a fundamental role in cardiovascular homeostasis in both physiological and pathological conditions, influencing cardiac contractility, heart rate (HR), diastolic function and systemic vascular resistance (SVR) through genomic and non-genomic mediated effects. In heart failure (HF) the main alteration of thyroid function is referred to as "low-triiodothyronine (T3) syndrome" (LT3S) characterized by decreased total serum T3 and free T3 (fT3) with normal levels of thyroxine (T4) and thyrotropin (TSH). Even if commonly interpreted as an adaptive factor, LT3S may have potential negative effects, contributing to the progressive deterioration of cardiac function and myocardial remodeling in HF and representing a powerful predictor of mortality in HF patients. All these observations, together with the early evidence of the benefits of T3 administration in HF patients indicate that placebo-controlled prospective studies are now needed to better define the safety and prognostic effects of chronic treatment with synthetic TH in HF.

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“…TH treatment appears not only to induce the expression of HSP27 in the cytoskeleton of the unstressed myocardium, but also to accelerate its translocation and phosphorylation to the cytoskeleton upon subsequent ischemic stress, indicating that TH can increase the tolerance of the heart by preserving cytoskeleton integrity [43]. This is further documented in studies with neonatal cardiomyocytes exposed to hypoxia [46].…”

Section: Clinical Implications: Protection Versus Functionmentioning

confidence: 91%

“…Furthermore, PKCd is shown to phosphorylate important cardioprotective molecules, such as heat shock protein 27 (HSP27) [41]. TH treatment resulted in increased expression and phosphorylation of PKCd and this response was associated with increased phosphorylation of the HSP27 and suppressed activation of the ischemiareperfusion p38 MAPK [42,43] (Fig. 2).…”

Section: Clinical Implications: Protection Versus Functionmentioning

confidence: 93%

Rebuilding the post-infarcted myocardium by activating ‘physiologic’ hypertrophic signaling pathways: the thyroid hormone paradigm

2008

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Viable myocardium undergoes several changes in the course of cardiac remodeling following myocardial infarction aiming to adapt the heart to the hemodynamic compromise. This response is characterized by reactivation of the fetal transcriptional program and results in cardiac dysfunction. Changes in thyroid hormone (TH)-TH receptors (TRs) axis occur in the course of post-infarction cardiac remodeling and seem to contribute to cardiac fetal phenotype. TH can "rebuild" the post-infarcted heart by preventing the fetal-like pattern of contractile proteins expression, normalizing wall tension, and optimizing cardiac chamber geometry. This effect seems to be attributed to TH pleiotropic cellular actions; TH promotes tissue growth and differentiation and favorably remodels cardiac cell while increases cellular survival upon stress. TH may constitute a new therapeutic option for mending the ischemic myocardium.

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Thyroxine pretreatment increases basal myocardial heat-shock protein 27 expression and accelerates translocation and phosphorylation of this protein upon ischaemia

Cited by 53 publications

References 34 publications

New insights into the role of thyroid hormone in cardiac remodeling: time to reconsider?

New insights into the role of thyroid hormone in cardiac remodeling: time to reconsider?

The role of thyroid hormone in the pathophysiology of heart failure: clinical evidence

Rebuilding the post-infarcted myocardium by activating ‘physiologic’ hypertrophic signaling pathways: the thyroid hormone paradigm

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