Alcohol-associated liver disease (ALD) encompasses a progressive pathological spectrum, ranging from steatosis to cirrhosis and hepatocellular carcinoma. Its development is driven by complex interactions among ethanol metabolism, oxidative stress, inflammation, fibrogenesis, and gut-liver axis dysregulation. Emerging evidence indicates that microRNAs (miRNAs) function as key posttranscriptional regulators that integrate metabolic reprogramming, immune responses, and fibrogenic signaling during ALD progression. This review summarizes the current understanding of miRNA biology and highlights their roles in lipid metabolism, oxidative stress responses, innate immune activation, and hepatic stellate cell-mediated fibrosis. Particular attention is given to context-dependent miRNAs, including miR-122, miR-34a, miR-155, miR-21, and the miR-29 family, whose functional effects vary by cell type and disease stage. We further discuss extracellular vesicles and exosome-associated miRNAs as mediators of intercellular communication and as minimally invasive biomarkers that reflect liver-derived injury signals rather than disease-specific signatures. Circulating miR-122 and miR-192 exemplify this concept, emphasizing the need for multi-miRNA panels integrated with clinical parameters to improve diagnostic specificity. Furthermore, therapeutic strategies targeting miRNAs―such as miRNA mimics, antagomirs, and locked nucleic acid inhibitors―have demonstrated promising preclinical efficacy in modulating steatosis, inflammation, and fibrosis. However, challenges such as off-target effects, delivery efficiency, and cell-type specificity remain major barriers to clinical translation. Overall, miRNAs represent a central molecular layer linking metabolic stress, immune dysregulation, and fibrogenesis in ALD. Future integration of multiomics and cell-specific delivery technologies might enable precision medicine approaches that leverage miRNA networks for early diagnosis and targeted therapy in ALD.

The biogenesis and biological roles of extracellular vesicles (EVs) in the progression of liver diseases have attracted considerable attention in recent years. EVs are membrane-bound nanosized vesicles found in different types of body fluids and contain various bioactive materials, including proteins, lipids, nucleic acids, and mitochondrial DNA. Based on their origin and biogenesis, EVs can be classified as apoptotic bodies, microvesicles, and exosomes. Among these, exosomes are the smallest EVs (30-150 nm in diameter), which play a significant role in cell-to-cell communication and epigenetic regulation. Moreover, exosomal content analysis can reveal the functional state of the parental cell. Therefore, exosomes can be applied to various purposes, including disease diagnosis and treatment, drug delivery, cell-free vaccines, and regenerative medicine. However, exosome-related research faces two major limitations: isolation of exosomes with high yield and purity and distinction of exosomes from other EVs (especially microvesicles). No standardized exosome isolation method has been established to date; however, various exosome isolation strategies have been proposed to investigate their biological roles. Exosome-mediated intercellular communications are known to be involved in alcoholic liver disease and nonalcoholic fatty liver disease development. Damaged hepatocytes or nonparenchymal cells release large numbers of exosomes that promote the progression of inflammation and fibrogenesis through interactions with neighboring cells. Exosomes are expected to provide insight on the progression of liver disease. Here, we review the biogenesis of exosomes, exosome isolation techniques, and biological roles of exosomes in alcoholic liver disease and nonalcoholic fatty liver disease.