Mitophagy is an evolutionarily highly conserved selective autophagy process that maintains cellular homeostasis and mitochondrial quality control by specifically recognizing and removing damaged or superfluous mitochondria. During tumorigenesis， mitophagy eliminates damaged mitochondria and reduces the accumulation of reactive oxygen species （ROS）， thereby helping to sustain cellular homeostasis. Energy metabolism refers to the core biological process through which cells convert chemical energy from nutrients into adenosine triphosphate （ATP） via biochemical pathways such as glycolysis and oxidative phosphorylation， providing energy for cellular activities. While research on gastrointestinal tumors is advancing rapidly， a major bottleneck lies in their complex metabolic adaptations and therapeutic resistance. Targeting the interplay between mitophagy and energy metabolism has emerged as a promising therapeutic strategy for this disease. Current research on mitophagy and energy metabolism in gastrointestinal tumors， including the molecular mechanisms of their bidirectional regulatory network and applications in targeted therapies， remains to be systematically elucidated. Therefore， this review summarizes the implications of the mitophagy-energy metabolism interplay in gastrointestinal tumors， with the aim of providing insights for future research.