miR-204: Molecular Regulation and Role in Cardiovascular and Renal Diseases.

miR-204: Molecular Regulation and Role in Cardiovascular and Renal Diseases.
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miR-204:心血管和肾脏疾病中的分子调控和作用。

DOI:
10.1161/hypertensionaha.121.14536
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发表时间:
2021-08
期刊:
Hypertension (Dallas, Tex. : 1979)
影响因子:
--
通讯作者:
Liang M
Liang M
中科院分区:
其他
文献类型:
--
作者:
Liu J;Liu Y;Wang F;Liang M

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microRNA研究领域已经从旨在衡量microRNA重要性的研究发展到专注于理解特定microRNA子集的研究,这些microRNA已成为分子系统和病理生理条件的有效调节剂。在这篇文章中,我们回顾了miR-204的分子特征和调控,以及越来越多的证据表明miR-204在心血管和肾脏生理和病理生理过程的调节中发挥重要作用。miR-204表现出高度组织特异性的表达模式,并且miR-204的丰度受到多种转录和转录后机制的调节。强有力的证据支持miR-204在减轻肺动脉高压和高血压和糖尿病肾损伤中的作用,同时在广泛的模型系统中促进高血压和内皮功能障碍。miR-204可能通过以组织特异性方式靶向几种生物学途径来影响这些疾病过程。miR-204在心血管和肾脏疾病患者中表达异常。明确的功能作用和明确的临床相关性表明miR-204是心血管和肾脏疾病中的高价值microRNA。
The field of microRNA research has evolved from studies aiming to gauge the importance of microRNAs to those focusing on understanding a subset of specific microRNAs that have emerged as potent regulators of molecular systems and pathophysiological conditions. In this article, we review the molecular features and regulation of miR-204 and the growing body of evidence for an important role of miR-204 in the regulation of cardiovascular and renal physiology and pathophysiological processes. miR-204 exhibits a highly tissue-specific expression pattern, and miR-204 abundance is regulated by several transcriptional and post-transcriptional mechanisms. Strong evidence supports a role for miR-204 in attenuating pulmonary arterial hypertension and hypertensive and diabetic renal injury while promoting hypertension and endothelial dysfunction in a wide range of model systems. miR-204 may influence these disease processes by targeting several biological pathways in a tissue-specific manner. miR-204 is dysregulated in patients with cardiovascular and renal diseases. The unequivocal functional roles and clear clinical relevance indicate that miR-204 is a high-value microRNA in cardiovascular and renal diseases.
DOI: 10.4103/2045-8932.114751
发表时间: 2013-04
影响因子: 2.6
作者:
von Gise A;Archer SL;Maclean MR;Hansmann G
通讯作者: Hansmann G