Mullath A, Krishna M. Role of long non-coding RNAs in non-alcoholic fatty liver disease. World J Meta-Anal 2024; 12(3): 97757 [DOI: 10.13105/wjma.v12.i3.97757]
Corresponding Author of This Article
Murali Krishna, DNB, MBBS, MD, Assistant Professor, Surgeon, Department of Urology, Army Hospital, R & R, Dhaula Kuan, New Delhi, Delhi Cantonment 110010, Delhi, India. murali276@yahoo.com
Research Domain of This Article
Gastroenterology & Hepatology
Article-Type of This Article
Editorial
Open-Access Policy of This Article
This article is an open-access article which was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/
World J Meta-Anal. Sep 18, 2024; 12(3): 97757 Published online Sep 18, 2024. doi: 10.13105/wjma.v12.i3.97757
Role of long non-coding RNAs in non-alcoholic fatty liver disease
Anju Mullath, Murali Krishna
Anju Mullath, Department of Gastroenterology, Aster Royal Hospital, Muscat 133, Muscat, Oman
Murali Krishna, Department of Urology, Army Hospital, R & R, Delhi Cantonment 110010, Delhi, India
Author contributions: Mullath A conceptualized and researched the study; Krishna M contributed to the research and wrote the manuscript.
Conflict-of-interest statement: All the authors declare that they have no conflict of interest.
Open-Access: This article is an open-access article that was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution NonCommercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: https://creativecommons.org/Licenses/by-nc/4.0/
Corresponding author: Murali Krishna, DNB, MBBS, MD, Assistant Professor, Surgeon, Department of Urology, Army Hospital, R & R, Dhaula Kuan, New Delhi, Delhi Cantonment 110010, Delhi, India. murali276@yahoo.com
Received: June 7, 2024 Revised: August 6, 2024 Accepted: August 15, 2024 Published online: September 18, 2024 Processing time: 98 Days and 3 Hours
Abstract
Non-alcoholic fatty liver disease (NAFLD) is emerging as a common cause of chronic liver disease in children and adults. NAFLD can progress to steatohepatitis and potentially even hepatocellular carcinoma. Early identification of patients at risk for progressive disease is crucial for managing NAFLD. Recent studies have identified long noncoding RNAs (lncRNAs), circular RNAs, and microRNAs as playing important roles in the pathogenesis of NAFLD. These noncoding RNAs are involved in modulating several metabolic pathways such as hepatic glucose and lipid metabolism, oxidative stress, and even carcinogenesis. Elevated levels of lncARSR and lncRNA nuclear-enriched abundant transcript 1 have been found in patients with NAFLD. In addition, lncRNAs such as PRYP4-3 and RP11-128N14.5 can distinguish patients with NAFLD from healthy individuals. Increased MEG3 expression has been observed in both NAFLD and non-alcoholic steatohepatitis, suggesting that it may help predict patients at risk for disease progression. With advances in transcriptomics, we may discover additional targets to help in the identification and prognostication of NAFLD.
Core Tip: Non-alcoholic fatty liver disease (NAFLD) is one of the most common liver ailments. Early diagnosis and treatment can help mitigate its impact on the liver. The role of long non-coding RNAs (lncRNAs) in the pathogenesis of NAFLD has been the subject of research for some time. LncRNAs such as plasmacytoma variant translocation 1, nuclear-enriched abundant transcript 1, muscle- and adipose-associated long intergenic non-coding RNA, and H19 have been shown to play important roles in the disease process of NAFLD.
