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

ABSTRACT

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.