Critical effects of long non-coding RNA on fibrosis diseases

The expression or dysfunction of long non-coding RNAs (lncRNAs) is closely related to various hereditary diseases, autoimmune diseases, metabolic diseases and tumors. LncRNAs were also recently recognized as functional regulators of fibrosis, which is a secondary process in many of these diseases and a primary pathology in fibrosis diseases. We review the latest findings on lncRNAs in fibrosis diseases of the liver, myocardium, kidney, lung and peritoneum. We also discuss the potential of disease-related lncRNAs as therapeutic targets for the clinical treatment of human fibrosis diseases. Fibrosis: Non-coding RNA as a cause for scar tissue Members of an enigmatic class of RNA molecules may offer useful targets for treating fibrosis. Fibrosis, the formation of scar tissue within an organ, is a damaging process which occurs in many different diseases, either as the primary disease or secondary to other conditions, for example various hereditary diseases, autoimmune diseases, metabolic diseases and tumors. Yue Zhang from the 105th Hospital of PLA, Hefei, and colleagues across China have reviewed the contributions of long non-coding RNAs to fibrosis in liver, myocardium, kidney, lung and peritoneum. These lncRNA molecules do not code for protein, but regulate the expression of other genes. There are many different lncRNAs that offer possible diagnostic indicators or targets for treatment of fibrosis.The molecular pathway underlying fibrosis is also associated with onset of cancer, and lncRNA-oriented therapeutics may therefore prove useful for oncology.