Pioneering Research in Medical Science: The Role of miR-93 in Liver Disease

In a groundbreaking step in medical research, a research team led by Professor Jang Hyun Choi from the Ulsan National Institute of Science and Technology (UNIST), in collaboration with Professor Huayong Yun from Pusan National University (PNU) and Professor Nyoung Hwa Park from Ulsan University Hospital (UUH), has identified the role of microRNA-93 (miR-93) as a key genetic regulator in the development of MASLD.

miR-93: A Genetic Regulator in Liver Cells

miR-93 refers to a specialized RNA molecule expressed in liver cells, functioning to inhibit the expression of specific target genes. The research team found abnormally high levels of miR-93 in both patients with fatty liver disease and animal models. Through molecular analysis, they demonstrated that miR-93 promotes fat accumulation, inflammation, and fibrosis by inhibiting the expression of the SIRT1 gene, which is involved in fat metabolism within liver cells.

Gene Editing Effects on miR-93

In experiments using gene editing techniques to eliminate miR-93 production in mice, researchers observed a significant reduction in liver fat accumulation, along with notable improvements in insulin sensitivity and liver function indicators. Conversely, mice with increased miR-93 expression showed deterioration in hepatic metabolic function.

Discovery of Niacin’s Role in Suppressing miR-93

Through screening 150 FDA-approved drugs, niacin (vitamin B3) was found to be the most effective in suppressing miR-93. Mice treated with niacin showed a significant decrease in liver miR-93 levels and a marked increase in SIRT1 activity. Active SIRT1 worked to restore disrupted fat metabolism pathways, thereby normalizing liver fat balance.

Clinical and Applied Dimensions of the Study

The research team explained that this study precisely elucidates the molecular origin of MASLD and demonstrates the potential to repurpose an already approved vitamin compound to modify this pathway, which holds high practical importance in clinical settings. They added that niacin, as a well-known and safe drug for treating hyperlipidemia, may hold promise as a candidate for combinatorial therapies targeting miRNA pathways in MASLD.

Conclusion

In conclusion, this study provided new insights into the role of miR-93 as a genetic regulator in MASLD and highlighted the promising potential of using niacin as a possible treatment. Supported by several institutions, including the National Research Foundation of Korea and the Korea Research Institute of Bioscience and Biotechnology, this research represents an important step toward a deeper understanding of liver diseases and the development of innovative therapeutic strategies. The publication of these findings in the prestigious biomedical journal “Metabolism: Clinical and Experimental” enhances its standing and significance in the scientific community.