Epigenetic influence of long non-coding steatogenic RNAs on the development of metabolic dysfunction-associated steatotic liver disease

Background. Metabolic dysfunction-associated steatotic liver disease (MASLD) is the most common chronic liver disease in humans, which is caused by changes in the expression level of long non-coding RNAs (lncRs). The aim of this literature review is to present a brief description of the role of steatogenic lncRs in the epigenetic influence on the development of MASLD, analyzing the data of modern scientific literature. Materials and methods. An analysis of 60 literature sources over the past five years was conducted from the databases MEDLINE; Embase; PreMedline In-Process & Other Non-Indexed Citations; The Cochrane Systematic Reviews Database, DARE, NHS EED and HTA databases; Web of Knowledge Science Citation Index; Web of Knowledge ISI Proceedings; CRD databases; BIOSIS, which were selected using the following keywords: long non-coding RNAs, epigenetic regulation, metabolically associated fatty liver disease, metabolic dysfunction-associated steatotic liver disease obesity. PROSPERO CRD420250652980. Results. Increased expression of steatogenic lncRs, such as CCAT1, Gm10804, Gm15622, H19, HOTAIR, lncARSR, NEAT1, PVT1, SRA, Uc.372, is a characteristic feature of the development and progression of hepatic steatosis in MASLD. The development of hepatic steatosis in MASLD is supported by a decrease in the expression level of anti-steatotic lncRs, including AC012668, FLRL2, Gm16551, lncHR1, B4GALT1-AS1/lncSHGL, MEG3, lncR MRAK052686. Conclusions. Long noncoding RNAs have an unconditional pathogenetic influence on the main mechanisms of the development of hepatic steatosis in MASLD, promoting lipid uptake in hepatocytes, enhancing de novo lipogenesis, inhibiting β-oxidation of fatty acids and lipid export from hepatocytes.