Lysosomes are not only the degradation center for substances in cells, but also an important metabolic sensor for many substances, metabolic processes, and cell growth. Similarly, mitochondria are the main metabolic centers that determine the fate of cells. Together, these two organelles jointly regulate cell metabolism through interactions with each other, and their dysfunction is closely related to metabolic diseases, neurodegenerative diseases, and lysosomal storage diseases. At present, we recognize that mitochondria interact with lysosomes through mitophagy, mitochondrial-derived vesicles, and mitochondrial-lysosomal membrane contact sites. However, the mechanisms regulating these pathways remains unclear. In recent years, Rab7 protein has been implicated in processes of mitochondria-lysosome crosstalk, including the formation of mitochondrial autophagosomes, fusion of mitochondrial autophagosomes with lysosomes, and mitochondrial- lysosome contact and dissociation. In this article, we review the role of Rab7 in crosstalk between mitochondria and lysosomes, which provides a new theoretical basis for disease involving mitochondrial and lysosomal dysfunction.