Abstract: Hypoxia is the pathophysiological basis of various diseases, stimulating a series of changes in lung tissue cells to adapt to the hypoxic microenvironment. Mitochondrial autophagy is a selective autophagy pathway similar to other autophagy pathways, which plays an important role in cellular stress. Recently, studies have conveyed that when cells are exposed to environmental stimuli such as low oxygen, a series of stress changes occur. Appropriate mitochondrial autophagy in the early stage of hypoxia can specifically clear damaged mitochondria and alleviate cell damage. However, with prolonged hypoxia, mitochondrial autophagy is promoted, mitochondrial function is damaged, and apoptosis is inhibited through activation of PINK1/ Parkin-mediated pathway, FUNDC1 receptor phosphorylation, and up-regulation of HIF-1α and ROS. Increase cell proliferation. Pulmonary tissues are most sensitive to oxygen concentration and in prolonged hypoxic environment, the pathophysiological changes of abnormal contraction of pulmonary vessels and remodeling of pulmonary arterioles would lead to increased pulmonary circulation resistance and hypoxic pulmonary hypertension (HPH). Mitophagy is closely related to its occurrence and development. Further research on the specific mechanism underlying hypoxia-induced mitophagy may provide new directions for the treatment of HPH. This article reviews the mechanisms behind hypoxia-induced mitophagy and its role in hypoxic-induced pulmonary hypertension along with recent research progress.