Role of MicroRNAs in Alcohol-Related Liver Disease

ABSTRACT

Alcohol-related liver disease (ARLD) is the most prevalent type of chronic liver disease and one of the most serious health problems worldwide. Individuals consuming more than 40 g of alcohol per day can develop alcoholic fatty liver (AFL). Progression of AFL to alcoholic steatohepatitis leading to ARLD. The risk factors such as oxidative stress, inflammatory response, and genetic and epigenetic factors might explain considerable variation in ARLD pathogenesis. Diagnosis of patients with ARLD involved assessing alcohol use disorder and signs of advanced liver disease. Increasing number of patients with advanced stages of ARLD is observed due to failure in early detection and treatment. Alcohol abstinence, nutritional therapy and corticosteroids are the best treatment for all stages of ARLD. Therapies targeting IL-22/STAT3, TNF receptor superfamily, antioxidant signal, LPS, inflammasomes, hormones and microRNAs are used in treatment of ARLD as translational research. MicroRNAs are non-coding RNAs mainly involved in underlying mechanisms of development and pathogenesis of ARLD. The current review summarizes the role of aberrant regulation of microRNAs involved during oxidative stress, epigenetic modulations and inflammatory response in ARLD and also focused on the underlying mechanism of microRNAs in different stages of liver diseases such as liver fibrosis, liver cirrhosis and hepatocellular carcinoma.

KEYWORDS:

• Alcohol abuse
• liver injury
• microRNAs
• liver fibrosis
• biomarkers

Acknowledgments

We (Authors) are thankful to DST for the funding support

Author contributions

Prabhudas Nelaturi, PhD and Sangeetha Prabhu Kademani, PhD; conceptualization, resources, and writing-original draft preparation. Krishna Sumanth Nallagangula, PhD; writing—review and editing. Sambandam Ravikumar, PhD; conceptualization, writing—review and editing, supervision.

Disclosure statement

The authors diclare no conflicts of interest.

Additional information

Funding

This work was supported by DST project: TPN/75989