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微小 RNA 与子宫内膜异位症中的血管生成。

MicroRNAs and angiogenesis in endometriosis.

机构信息

Instituto de Investigación Sanitaria La Fe, Hospital Universitario y Politécnico La Fe, Valencia, Spain.

Area Maternoinfantil, Hospital General Universitario, Valencia, Spain.

出版信息

Thromb Res. 2015 Feb;135 Suppl 1:S38-40. doi: 10.1016/S0049-3848(15)50439-8. Epub 2015 Feb 9.

DOI:10.1016/S0049-3848(15)50439-8
PMID:25903532
Abstract

miRNAs function as important regulators of a wide range of cellular processes, such as angiogenesis and fibrinolysis, by postranscriptional modulation of gene expression. We present a review on the role of miRNAs and angiogenesis in endometriosis. Endometriosis, defined as the implantation of endometrial tissue outside the uterine cavity, is one of the most frequent benign gynecological diseases and it has important consequences on the quality of life and fertility of patients. Similarly to tumor metastasis, the ectopic endometrium acquires the capability to adhere, proliferate and infiltrate the extracellular matrix. Endometriosis is a multifactorial and polygenic disease in which angiogenesis and proteolysis may be involved, and emerging data provide evidence that a dysregulation of miRNA expression may be implicated in these processes. The detection of circulating miRNAs in plasma and other body fluids and their relative stability has raised the possibility that they might serve as non-invasive biomarkers for the diagnosis of the disease. On the other hand, the development of therapies that might block the expression or mimic the functions of miRNAs could represent new therapeutic strategies for the treatment of endometriosis.

摘要

miRNAs 通过对基因表达的转录后调控,作为广泛的细胞过程(如血管生成和纤维蛋白溶解)的重要调节剂发挥作用。我们就 miRNAs 和血管生成在子宫内膜异位症中的作用进行综述。子宫内膜异位症是指子宫内膜组织在子宫腔外的植入,是最常见的良性妇科疾病之一,对患者的生活质量和生育能力有重要影响。与肿瘤转移类似,异位子宫内膜获得了黏附、增殖和浸润细胞外基质的能力。子宫内膜异位症是一种多因素和多基因疾病,其中血管生成和蛋白水解可能涉及,并且新出现的数据提供了证据表明 miRNA 表达的失调可能与这些过程有关。在血浆和其他体液中检测到循环 miRNAs 及其相对稳定性,使得它们可能成为该疾病诊断的非侵入性生物标志物。另一方面,开发可能阻断 miRNA 表达或模拟其功能的疗法可能代表治疗子宫内膜异位症的新治疗策略。

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Thromb Res. 2015 Feb;135 Suppl 1:S38-40. doi: 10.1016/S0049-3848(15)50439-8. Epub 2015 Feb 9.
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