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MicroRNAs in liver fibrosis: Focusing on the interaction with hedgehog signaling
1Jeongeun Hyun, Youngmi Jung, Department of Biological Sciences, College of Natural Science, Pusan National University, Pusan 46241, South Korea.
Abstract:
Liver fibrosis is a repair process in response to damage in the liver; however, severe and chronic injury promotes the accumulation of fibrous matrix, destroying the normal functions and architecture of liver. Hepatic stellate cells (HSCs) are quiescent in normal livers, but in damaged livers, they transdifferentiate into myofibroblastic HSCs, which produce extracellular matrix proteins. Hedgehog (Hh) signaling orchestrates tissue reconstruction in damaged livers and contributes to liver fibrogenesis by regulating HSC activation. MicroRNAs (miRNAs), endogenous small non-coding RNAs interfering with RNA post-transcriptionally, regulate various cellular processes in healthy organisms. The dysregulation of miRNAs is closely associated with diseases, including liver diseases. Thus, miRNAs are good targets in the diagnosis and treatment of various diseases, including liver fibrosis; however, the regulatory mechanisms of miRNAs that interact with Hh signaling in liver fibrosis remain unclear. We review growing evidence showing the association of miRNAs with Hh signaling. Recent studies suggest that Hh-regulating miRNAs induce inactivation of HSCs, leading to decreased hepatic fibrosis. Although miRNA-delivery systems and further knowledge of interacting miRNAs with Hh signaling need to be improved for the clinical usage of miRNAs, recent findings indicate that the miRNAs regulating Hh signaling are promising therapeutic agents for treating liver fibrosis.
Insights
MicroRNAs (miRNAs) regulate Hedgehog (Hh) signaling to inactivate hepatic stellate cells (HSCs), reducing liver fibrosis. These Hh-regulating miRNAs show promise as novel therapeutics for liver fibrosis.
Area of Science:
- Hepatology
- Molecular Biology
- Biochemistry
Background:
- Liver fibrosis results from chronic liver injury, leading to scar tissue accumulation and impaired liver function.
- Hepatic stellate cells (HSCs) activate into myofibroblasts, producing extracellular matrix and driving fibrogenesis.
- Hedgehog (Hh) signaling is crucial for liver repair but also promotes fibrosis by activating HSCs.
Purpose of the Study:
- To review the role of microRNAs (miRNAs) in regulating Hh signaling during liver fibrosis.
- To explore the therapeutic potential of miRNAs targeting Hh signaling for liver fibrosis treatment.
Main Methods:
- Literature review of studies investigating miRNA and Hh signaling interactions in liver fibrosis.
- Analysis of evidence linking miRNA dysregulation to HSC activation and fibrogenesis.
- Evaluation of recent findings on Hh-regulating miRNAs in preclinical models.
Main Results:
- MicroRNAs (miRNAs) are endogenous regulators of gene expression implicated in liver diseases.
- Dysregulated miRNAs are associated with liver fibrosis, impacting HSC activation.
- Hh-signaling-regulating miRNAs have been shown to inactivate HSCs, thereby decreasing hepatic fibrosis.
Conclusions:
- MicroRNAs targeting Hh signaling represent a promising therapeutic strategy for liver fibrosis.
- Further development of miRNA delivery systems and understanding of miRNA-Hh interactions are needed for clinical application.
- Hh-regulating miRNAs offer a novel approach to combat liver fibrosis by modulating HSC activity.
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