The mechanisms and therapeutic potential of long noncoding RNA NEAT1 in fibrosis

被引:7
作者
Jiang, Xiaoying [1 ]
机构
[1] Xi An Jiao Tong Univ, Sch Basic Med Sci, Dept Biochem & Mol Biol, Hlth Sci Ctr, 76 Yanta West Rd, Xian 710061, Shaanxi, Peoples R China
基金
美国国家科学基金会;
关键词
Fibrosis; Long noncoding RNAs; NEAT1; Therapeutic target; DIABETIC-NEPHROPATHY; PROGRESSION; LIVER;
D O I
10.1007/s10238-023-01191-1
中图分类号
R-3 [医学研究方法]; R3 [基础医学];
学科分类号
1001 ;
摘要
Fibrosis is the excess deposition of extracellular matrix involved in the pathogenesis of chronic diseases and finally leads to the disruption of tissue architecture and failure of organ function. Long noncoding RNAs (lncRNAs) are a class of RNAs with lengths greater than 200 nucleotides and do not code proteins, which regulate gene expression at multiple levels. Nuclear-enriched abundant transcript 1 (NEAT1) is a long noncoding RNA that is widely expressed in mammalian cells and known as essential architectural scaffold for the formation of paraspeckles. Recently, the accumulating studies demonstrated that lncRNA NEAT1 was remarkable upregulated in the development of fibrosis in different organs, such as liver fibrosis, renal fibrosis, cardiac fibrosis, and lung fibrosis. More importantly, knockdown of NEAT1 remarkably alleviated fibrosis in vitro and in vivo. In this review, we summarized current studies of NEAT1 in fibrosis and hopefully aid in a better understanding of the mechanisms of fibrosis and the potential of NEAT1 as novel therapeutic target for fibrosis.
引用
收藏
页码:3339 / 3347
页数:9
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