Abstract
Many studies have made clear that most of the genome is transcribed into noncoding RNAs, including microRNAs (miRNAs) and long noncoding RNAs (lncRNAs), both of which can affect different cell features. LncRNAs are long heterogeneous RNAs that regulate gene expression and a variety of signaling pathways involved in cellular homeostasis and development. Several studies have demonstrated that lncRNA is an important class of regulatory molecule that can be targeted to change cellular physiology and function. The expression or dysfunction of lncRNAs is closely related to various hereditary, autoimmune, and metabolic diseases, and tumors. Specifically, recent work has shown that lncRNAs have an important role in kidney pathogenesis. The effective roles of lncRNAs have been recognized in renal ischemia, injury, inflammation, fibrosis, glomerular diseases, renal transplantation, and renal-cell carcinoma. The present review focuses on the emerging role and function of lncRNAs in the pathogenesis of kidney inflammation and fibrosis as novel essential regulators. Although lncRNAs are important players in the initiation and progression of many pathological processes, their role in renal fibrosis remains unclear. This review summarizes the current understanding of lncRNAs in the pathogenesis of kidney fibrosis and elucidates the potential role of these novel regulatory molecules as therapeutic targets for the clinical treatment of kidney inflammation and fibrosis.
Highlights
Data analyses from genome projects have shown that less than 2% of transcribed genes encode protein-coding RNA, and that most noncoding transcripts are more than 200 base pairs and make up a group of long noncoding RNA [1,2,3]
The regulated on activation normal T-cell-expressed and secreted (RANTES) long noncoding RNAs (lncRNAs) is produced by renal tubular epithelial cells and acts as an inflammatory mediator in acute kidney injury (AKI) following ischemic reperfusion [48]
It was reported that some lncRNAs, including TrAnscript Predicting Survival in AKI (TapSAKI), psoriasis-associated RNA induced by stress, are involved in the pathogenesis of AKI, and have potential as diagnostic biomarkers [85,86]
Summary
Data analyses from genome projects have shown that less than 2% of transcribed genes encode protein-coding RNA, and that most noncoding transcripts are more than 200 base pairs and make up a group of long noncoding RNA (lncRNA) [1,2,3]. Huang et al [23] reported that lncRNA, activated by TGF-β1, is a promising biomarker in predicting the acute rejection (AR) of renal allografts. Their underlying mechanisms are still poorly understood. Understanding the molecular mechanism of lncRNAs in pathophysiological kidney processes may contribute to developing more effective therapeutics to prevent renal fibrosis.
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