Retard or exacerbate: Role of long non-coding RNA growth arrest-specific 5 in the fibrosis

被引:7
|
作者
Xiang, Zhang [1 ]
Liqing, Ye [1 ]
Qingqing, Ye [1 ]
Qiang, He [1 ]
Hongbo, Chen [1 ,2 ]
机构
[1] First Affiliated Hosp Zhejiang Chinese Med Univ, Hangzhou 310006, Peoples R China
[2] First Affiliated Hosp Zhejiang Chinese Med Univ, Dept Nephrol, Hangzhou 310006, Peoples R China
基金
中国国家自然科学基金;
关键词
LncRNA Gas5; Organ fibrosis; Function; Mechanism; NF-KAPPA-B; LNCRNA GAS5; CELL-PROLIFERATION; PROSTATE-CANCER; INHIBITION; EXPRESSION; GENE; ACTIVATION; MECHANISMS; APOPTOSIS;
D O I
10.1016/j.cytogfr.2022.06.001
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Fibrosis is the endpoint of pathological remodeling involving different expressions of non-coding RNA(ncRNA) including long non-coding RNA growth arrest-specific 5 (lncRNA Gas5). Up to now, many studies have demonstrated that lncRNA Gas5 may play a vital regulatory role in the occurrence and development of organ fibrosis including liver, renal and cardiac fibrosis et al. Furthermore, Gas5 may also serve as a biomarker in diagnostic settings for fibrosis diseases. Structurally, IncRNA Gas5 impacts fibrosis via its distinct structural modules. In response to various external stresses, distinct functional complexes on different parts of Gas5 sequence influence cell proliferation and survival, thus affecting the inflammatory process and deposition of extracellular matrix(ECM) in organ fibrosis. However, there is no consensus on the role of Gas5 in fibrosis and its changed expression under various circumstances. In this review, we present an overview of what is known about the effect of Gas5 in organ fibrosis so far and for the first time explain its mechanism in the progression of fibrosis based on its unique structure.
引用
收藏
页码:89 / 104
页数:16
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