Abstract
Dilated cardiomyopathy (DCM) is the most prevalent cardiomyopathy, typified by left ventricular dilation and systolic dysfunction. Many patients with DCM have altered thyroid status, especially lower levels of free triiodothyronine (T3) and elevated levels of thyroid-stimulating hormone. Moreover, growing evidence indicates that even subtle changes in thyroid status (especially low T3) are linked with a worse long-term prognosis and a higher risk of mortality. Notably, recent discoveries have shown that not only local myocardial thyroid hormones (THs) bioavailability could be diminished due to impaired expression of the activating deiodinase, but virtually all genes involved in TH biosynthesis are also expressed in the myocardium of DCM patients. Importantly, some studies have suggested beneficial effects of TH therapy in patients suffering from DCM. Our aim was to discuss new insights into the association between TH status and prognosis in DCM, abnormal expression of genes involved in the myocardial synthesis of TH in DCM, and the potential for TH use in the future treatment of DCM.
Highlights
Dilated cardiomyopathy (DCM), the most common form of cardiomyopathy, can be characterized as a nonischemic heart muscle disease with a structural and functional myocardial alteration
Genomic cellular effects of Thyroid hormones (THs) are triggered by T3, which binds to specific thyroid hormone receptors (THRs) in the nucleus
A large number of studies suggested that the appropriate function of thyroid glands is relevant in patients with DCM as thyroid dysfunction worsens cardiac function and raises the risk of overall mortality
Summary
Dilated cardiomyopathy (DCM), the most common form of cardiomyopathy, can be characterized as a nonischemic heart muscle disease with a structural and functional myocardial alteration. Thyroid hormones (THs) have direct and indirect effects on cardiac function. These effects are mediated by both genomic and nongenomic mechanisms. Binds to a specific nuclear receptor, which regulates the transcription of various genes responsible for proper cardiovascular function. Genomic cellular effects of THs are triggered by T3, which binds to specific thyroid hormone receptors (THRs) in the nucleus. THRs are able to regulate transcription via binding to thyroid hormone response elements (TREs). In the nucleus of cardiomyocytes, which regulates transcripinclude T3 binding to thyroid hormone receptor (THR) in the nucleus of cardiomyocytes, which regulates transcription tion of various genes by binding to thyroid hormone response elements (TREs). Nongenomic cellular pathways involve of various genes by binding to thyroid hormone response elements (TREs). Kinase, PI3-kinase—phosphatidylinositol 3-kinase, AKT—protein kinase B, NO—nitric oxide, EPO—erythropoietin, LV—
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