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循环肾素-血管紧张素-醛固酮相关 microRNAs 在甲状腺毒症性心脏病患者中的表达。

Expression of Circulating Rennin-Angiotensin-Aldosterone-Related microRNAs in Patients with Thyrotoxic Heart Disease.

机构信息

Guilin Medical University, Guilin, Guangxi Province, China.

Department of Endocrinology, Wuhan Union Hospital Affiliated to Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.

出版信息

Bull Exp Biol Med. 2021 Dec;172(2):125-132. doi: 10.1007/s10517-021-05348-4. Epub 2021 Dec 2.

DOI:10.1007/s10517-021-05348-4
PMID:34855075
Abstract

Thyrotoxic heart disease (THD) is a common and severe complication of hyperthyroidism and the etiology of this complication remains poorly understood. Activation of the rennin-angiotensin- aldosterone system by excess thyroxin is one of the major factors that contribute to the pathogenesis of THD. Several microRNAs such as miR-21, miR-155, miR-208a, and miR-499 are closely related to the rennin-angiotensin-aldosterone system and therefore should be involved in this process. Our study intends to explore whether these miRNAs are involved in the pathogenesis of THD, and if these miRNAs could be secreted into the circulation and serve as sentinel indicators for THD. Though there is a trend of elevation of miR- 155 in THD than in simple hyperthyroidism patients, we did not find statistically significant differences in the expression of these miRNAs in the blood of THD patients, but we found that miR-155 was significantly up-regulated in patients with Graves' disease with or without THD in comparison with healthy controls. Thus, miR-155 can serve as a novel biomarker for Graves' disease and can play important roles in pathogenesis of Graves' disease.

摘要

甲状腺毒症性心脏病(THD)是甲状腺功能亢进症的一种常见且严重的并发症,其病因仍知之甚少。过量甲状腺素激活肾素-血管紧张素-醛固酮系统是导致 THD 发病机制的主要因素之一。几种 microRNA 如 miR-21、miR-155、miR-208a 和 miR-499 与肾素-血管紧张素-醛固酮系统密切相关,因此应该参与这个过程。我们的研究旨在探讨这些 microRNA 是否参与 THD 的发病机制,以及这些 microRNA 是否可以分泌到循环中并作为 THD 的哨兵指标。虽然 THD 患者的 miR-155 呈升高趋势,但我们并未发现 THD 患者血液中这些 microRNA 的表达有统计学差异,但我们发现 Graves 病患者(无论是否伴有 THD)的 miR-155 均显著上调,与健康对照组相比。因此,miR-155 可以作为 Graves 病的新型生物标志物,在 Graves 病的发病机制中发挥重要作用。

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[Blockade of the renin-angiotensin-aldosterone system in Graves' disease].
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本文引用的文献

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Activation of the STAT3/microRNA-21 pathway participates in angiotensin II-induced angiogenesis.STAT3/miRNA-21 通路的激活参与了血管紧张素 II 诱导的血管生成。
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一个用于评估自身免疫性甲状腺疾病风险和严重程度的 MicroRNA 特征。
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AT1 receptor blockage impairs NF-κB activation mediated by thyroid hormone in cardiomyocytes.血管紧张素 II 型受体阻断可损害甲状腺激素在心肌细胞中介导的 NF-κB 激活。
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Intraindividual variation of microRNA expression levels in plasma and peripheral blood mononuclear cells and the associations of these levels with the pathogenesis of autoimmune thyroid diseases.血浆和外周血单个核细胞中微小RNA表达水平的个体内变异及其与自身免疫性甲状腺疾病发病机制的关联。
Clin Chem Lab Med. 2017 May 1;55(5):626-635. doi: 10.1515/cclm-2016-0449.
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MicroRNA-1 overexpression blunts cardiomyocyte hypertrophy elicited by thyroid hormone.miRNA-1 过表达可减轻甲状腺激素引起的心肌细胞肥大。
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Identifying circulating microRNAs as biomarkers of cardiovascular disease: a systematic review.将循环微RNA鉴定为心血管疾病的生物标志物:一项系统综述。
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Increased microRNA-155 and decreased microRNA-146a may promote ocular inflammation and proliferation in Graves' ophthalmopathy.微小RNA-155升高和微小RNA-146a降低可能促进格雷夫斯眼病的眼部炎症和增殖。
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MiRNA-208a and miRNA-208b are triggered in thyroid hormone-induced cardiac hypertrophy - role of type 1 Angiotensin II receptor (AT1R) on miRNA-208a/α-MHC modulation.甲状腺激素诱导的心肌肥厚中触发的 miRNA-208a 和 miRNA-208b-1 型血管紧张素 II 受体 (AT1R) 对 miRNA-208a/α-MHC 调节的作用。
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