Abstract
microRNAs (miRNAs) are small non-coding RNAs that regulate gene expression by either blocking translation or inducing degradation of target mRNA. miRNAs play essential roles in diverse biological and pathological processes, including development of hepatic fibrosis. Hepatic stellate cells (HSCs) play a central role in development of hepatic fibrosis and there are intricate regulatory effects of miRNAs on their activation, proliferation, collagen production, migration, and apoptosis. There are multiple differentially expressed miRNAs in activated HSCs, and in this review we aim to summarize current data on miRNAs that participate in the development of hepatic fibrosis. Based on this review, miRNAs may serve as biomarkers for diagnosis of liver disease, as well as markers of disease progression. Most importantly, dysregulated miRNAs may potentially be targeted by novel therapies to treat and reverse progression of hepatic fibrosis.
Highlights
Hepatic fibrosis ensues secondary to chronic hepatic injury and inflammation and some of the common etiologies are viral and autoimmune hepatitis, alcohol consumption, nonalcoholic steatohepatitis (NASH), metabolic diseases leading to copper or iron overload, toxins, and biliary obstruction [1,2]
There have been approximately 1880 miRNAs identified in homo sapiens, with each miRNA thought to target on average 200 transcripts; regulating up to one third of human genes [8,9,10]. miRNAs play an essential role in gene expression and regulate various biological processes such as cell differentiation, apoptosis, metabolism, and endocrine function [11,12,13,14]
Since chronic liver diseases and fibrosis are linked to the development of hepatocellular carcinoma (HCC), there has been increasing interest in studying Hepatic stellate cells (HSCs) as potential targets for treatment and prevention of hepatic fibrosis and development of HCC [2,35,36,37,38]
Summary
Hepatic fibrosis ensues secondary to chronic hepatic injury and inflammation and some of the common etiologies are viral and autoimmune hepatitis, alcohol consumption, nonalcoholic steatohepatitis (NASH), metabolic diseases leading to copper or iron overload, toxins, and biliary obstruction [1,2]. They discovered a small non-coding transcript of lin-4 gene that interacted with lin-4 messenger RNA (mRNA) and regulated translation and controlled post-embryonic development of c. They are approximately 20–27 nucleotides long and function as regulatory molecules by binding to target mRNA in the 31 -untranslated region (31 -UTR) leading to either repression of mRNA translation or promoting degradation [6,7]. Since their discovery, there have been approximately 1880 miRNAs identified in homo sapiens, with each miRNA thought to target on average 200 transcripts; regulating up to one third of human genes [8,9,10]. Single-stranded mature miRNAs interact with Argonaute (ARO) protein and is degraded in the RNA-induced silencing complex (RISC), which in turn modulates mRNA degradation and repression or activation of translation [24]
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