Lipid droplet–mitochondria contact sites are important membrane contact sites that connect lipid storage, fatty acid oxidation, and mitochondrial homeostasis. As the liver is responsible for lipid synthesis, storage, oxidation, and export, it provides an ideal setting for investigating the roles of these contact sites in physiological adaptation and pathological remodeling. Growing evidence suggests that, both in chronic lipid overload-induced hepatic metabolic injury and in acute hepatic ischemia-reperfusion injury, lipid droplet–mitochondria contact sites are positioned at the intersection of lipid flux regulation, mitochondrial stress thresholds, and inflammatory injury amplification. During the early stage of metabolic stress, moderate lipid droplet formation and lipid droplet–mitochondria coupling may facilitate lipid sequestration, fatty acid partitioning, and energy adaptation. However, under persistent lipid burden or reperfusion-associated oxidative stress, a mismatch between lipid droplet mobilization and mitochondrial uptake/oxidative capacity may lead to amplified lipotoxicity, reactive oxygen species bursts, mitochondrial DNA leakage, and sterile inflammation. In recent years, advances in super-resolution imaging, proximity labeling and spatial proteomics have promoted a shift in this field from morphological colocalization studies toward closed-loop analyses of structure, composition, and function. This review summarizes the structural basis and functional heterogeneity of lipid droplet–mitochondria contact sites, as well as their roles in hepatic metabolic injury and ischemia-reperfusion injury, and discusses their translational potential as disease stratification markers and therapeutic targets. Key words: lipid droplet; mitochondria; membrane contact site; hepatic metabolic injury; ischemia-reperfusion injury; lipotoxicity; mitochondrial homeostasis