The long noncoding RNA (lncRNA) myocardial infarction-associated transcript (MIAT) has emerged as a potential regulator of the pathogenesis of various liver diseases, including hepatocellular carcinoma (HCC), liver fibrosis, cirrhosis, nonalcoholic fatty liver disease (NAFLD), nonalcoholic steatohepatitis (NASH), chronic hepatitis C virus (HCV) infection, and chronic liver disease (CLD). This review summarizes evidence showing that MIAT is overexpressed in liver disease tissues, both in human patients and in animal models. In these contexts, MIAT functions as a competing endogenous RNA (ceRNA), sponging microRNAs such as miR-3085-5p, miR-214, miR-411-5p, miR-520d-3p, miR-22-3p, and miR-149-5p. These interactions activate key signaling pathways, including the Hippo/YAP, Wnt/β-catenin, TGF-β/Smad, PI3K/AKT, NF-κB, and STAT3/PD-L1 pathways which collectively promote HSCs activation, epithelial mesenchymal transition (EMT), extracellular matrix (ECM) deposition, and cell proliferation. In HCC, MIAT expression is correlated with advanced tumor stage, poor clinical prognosis, and resistance to targeted therapies such as sorafenib. In liver fibrosis and other CLDs, MIAT sustains inflammatory and oxidative stress responses, thereby linking diverse etiologies, including viral infection and metabolic syndrome. Moreover, MIAT modulates hepatitis C virus (HCV) replication by suppressing innate immune signaling through RIG-I/IRF3 inhibition while enhancing hepatic lipogenesis. Unlike other lncRNAs, such as H19, NEAT1, and TUG1, MIAT uniquely integrates inflammatory, fibrogenic, and oncogenic pathways. Circulating MIAT can also serve as a noninvasive biomarker for early diagnosis and prognostic assessment. Therapeutically, MIAT silencing via siRNAs, antisense oligonucleotides (ASOs), or CRISPR-based strategies has demonstrated both antifibrotic and antitumor efficacy in preclinical models. Key limitations include disease-specific variability and insufficient validation in human studies.