N ⁶ ‐Methyladenosine (m ⁶ A) in Liver Disease: Pathogenic Mechanisms and Therapeutic Potential

Accumulating evidence highlights the critical role of epigenetic modifications, particularly N 6 ‐methyladenosine (m 6 A), in liver disease. As the most abundant RNA modification in eukaryotic cells, m 6 A is dynamically regulated by multicomponent m 6 A methyltransferases (e.g., METTL3 and METTL14), demethylases (FTO and ALKBH5), and m 6 A‐binding proteins (YTHDF1/2/3, YTHDC1/2, and IGF2BP1/2/3). Recent studies have revealed the pivotal involvement of m 6 A and its regulators in a wide range of physiological and pathological processes in liver disease, including metabolic dysfunction‐associated steatotic liver disease (MASLD), liver fibrosis, hepatocellular carcinoma (HCC), as well as liver injury and regeneration. In this review, we summarize recent advances in understanding the emerging roles of m 6 A modifications in liver disease and discuss their potential as therapeutic targets, offering new perspectives for treating liver disease.