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甲状腺激素介导的心脏保护机制的新见解。

New insights into mechanisms of cardioprotection mediated by thyroid hormones.

作者信息

Nicolini G, Pitto L, Kusmic C, Balzan S, Sabatino L, Iervasi G, Forini F

机构信息

Institute of Clinical Physiology, CNR, 56100 Pisa, Italy ; CNR, Tuscany Region G. Monasterio Foundation, Pisa, Italy.

出版信息

J Thyroid Res. 2013;2013:264387. doi: 10.1155/2013/264387. Epub 2013 Mar 10.

DOI:10.1155/2013/264387
PMID:23555069
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3608184/
Abstract

Heart failure represents the final common outcome in cardiovascular diseases. Despite significant therapeutic advances, morbidity and mortality of heart failure remain unacceptably high. Heart failure is preceded and sustained by a process of structural remodeling of the entire cardiac tissue architecture. Prevention or limitation of cardiac remodeling in the early stages of the process is a crucial step in order to ameliorate patient prognosis. Acquisition of novel pathophysiological mechanisms of cardiac remodeling is therefore required to develop more efficacious therapeutic strategies. Among all neuroendocrine systems, thyroid hormone seems to play a major homeostatic role in cardiovascular system. In these years, accumulating evidence shows that the "low triiodothyronine" syndrome is a strong prognostic, independent predictor of death in patients affected by both acute and chronic heart disease. In experimental models of cardiac hypertrophy or myocardial infarction, alterations in the thyroid hormone signaling, concerning cardiac mitochondrion, cardiac interstitium, and vasculature, have been suggested to be related to heart dysfunction. The aim of this brief paper is to highlight new developments in understanding the cardioprotective role of thyroid hormone in reverting regulatory networks involved in adverse cardiac remodeling. Furthermore, new recent advances on the role of specific miRNAs in thyroid hormone regulation at mitochondrion and interstitial level are also discussed.

摘要

心力衰竭是心血管疾病的最终共同结局。尽管治疗取得了重大进展,但心力衰竭的发病率和死亡率仍然高得令人难以接受。在整个心脏组织结构的结构重塑过程之前及过程中,心力衰竭持续存在。在该过程的早期阶段预防或限制心脏重塑是改善患者预后的关键步骤。因此,需要获得心脏重塑的新病理生理机制,以制定更有效的治疗策略。在所有神经内分泌系统中,甲状腺激素似乎在心血管系统中发挥着主要的稳态作用。近年来,越来越多的证据表明,“低三碘甲状腺原氨酸”综合征是急性和慢性心脏病患者死亡的一个强有力的预后指标,且具有独立性。在心脏肥大或心肌梗死的实验模型中,甲状腺激素信号在心脏线粒体、心脏间质和血管方面的改变被认为与心脏功能障碍有关。这篇短文的目的是强调在理解甲状腺激素在逆转参与不良心脏重塑的调节网络中的心脏保护作用方面的新进展。此外,还讨论了特定微小RNA在线粒体和间质水平上对甲状腺激素调节作用的最新进展。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/743f/3608184/49039e3645b8/JTR2013-264387.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/743f/3608184/49039e3645b8/JTR2013-264387.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/743f/3608184/49039e3645b8/JTR2013-264387.001.jpg

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A low fT3 level as a prognostic marker in patients with acute myocardial infarctions.低游离三碘甲状腺原氨酸水平作为急性心肌梗死患者的预后标志物。
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