Decrypting the crosstalk of noncoding RNAs in the progression of IPF

Yujuan Wang,Rong Gao,Jin Ren,Han Li,Fenglian Zhao,Han Xiao,Bingdi Yan,Junling Yang

doi:10.1007/s11033-020-05368-9

Abstract

Idiopathic pulmonary fibrosis (IPF) is an agnogenic, rare, and lethal disease, with high mortality and poor prognosis and a median survival time as short as 3 to 5 years after diagnosis. No effective therapeutic drugs are still not available not only in clinical practice, but also in preclinical phases. To better and deeper understand pulmonary fibrosis will provide more effective strategies for therapy. Mounting evidence suggests that noncoding RNAs (ncRNAs) and their interactions may contribute to lung fibrosis; however, the mechanisms underlying their roles are largely unknown. In this review, we systematically summarized the recent advances regarding the crucial roles of long non-coding RNAs (lncRNAs), microRNAs (miRNAs), and circular RNAs (circRNAs) and crosstalk among them in the development of IPF. The perspective for related genes was well highlighted. In summary, ncRNA and their interactions play a key regulatory part in the progression of IPF and are bound to provide us with new diagnostic and therapeutic targets.

Highlights

Idiopathic pulmonary fibrosis (IPF) remains a chronic, debilitating, progressive pulmonary parenchyma illness, which falls under idiopathic interstitial pneumonia (IIP)
With the discovery of noncoding RNAs (ncRNAs) in the 1960’s, we identified its involvement in gene expression at transcription or post-transcription level, through epigenetics. ncRNAs constitute 98% of the human genome and are transcribed from the genome, but do not encode proteins
It can be categorized into long non-coding RNAs (lncRNAs), miRNAs, circRNAs, and other ncRNAs that differ in structure, size, and function. ncRNAs can modulate protein abundance by modifying transcription

Summary

Introduction

IPF remains a chronic, debilitating, progressive pulmonary parenchyma illness, which falls under idiopathic interstitial pneumonia (IIP). The circRNA/miRNA regulatory network is involved in many signaling pathways of lung fibrosis, like transforming growth factor (TGFβ1) and NF-κB, which effects cell propagation, motility, migration and collagen compound in IPF [43]. Hsa_circRNA_101996 can act as the molecular sponge of miR9 and 145, to regulate lung fibrosis via several signaling pathways, like the plateletderived growth factor receptor β (PDGFR-β) pathway [80, 81]. MiR-7 targets PAK1 and FAK1, verifying the abovementioned assumptions [86, 87] These results prove that circRNAs can form a series of post-transcriptional regulatory factors through its interaction with miRNAs. Compared with linear RNAs, more stable circRNAs are attractive for researchers who concentrate on biotechnological and therapeutic applications. STAT signaling pathway Involved in lung epithelial cell damage and fibroblast proliferation Binding to fibroblast growth factor receptor In a transacting form to affect the expression of most genes [73] [79] [80, 81] [64, 73]

Conclusion

Findings

Compliance with ethical standards