Hypoxic pulmonary hypertension at high altitude is a complicated pathophysiological condition and clinical syndrome that occurs after exposure to high altitude. As one of the major types of pulmonary hypertension, high-altitude hypoxic pulmonary hypertension poses a serious threat to the health of residents in plateau areas, with an increased risk of right heart failure and even premature death. However, the exact pathogenesis of hypoxic pulmonary hypertension, including high-altitude hypoxic pulmonary hypertension, has not been fully clarified, effective drugs for treatment still lacking. Recent studies have shown that iron deficiency is prevalent in patients with all types of pulmonary hypertension, and iron affects the expression of hypoxia-inducible factors (HIFs) target genes by regulating the activity of HIFs. Furthermore, iron participates in the biosynthesis of mitochondrial iron-sulfur clusters and regulates the generation of cellular reactive oxygen species (ROS), thereby modulating the occurrence and progression of hypoxic pulmonary hypertension. More intriguingly, there exists an important molecular dialogue between iron and hypoxia. Taken together, we hold the opinion that iron homeostasis may be involved in regulating the occurrence and development of hypoxic pulmonary hypertension, and the regulation of iron metabolism may represent a potential target for the intervention of hypoxic pulmonary hypertension. This article briefly reviewed iron homeostasis, iron metabolism disorders and hypoxic pulmonary hypertension, as well as the possible mechanisms by which the intervention of iron metabolism regulates hypoxic pulmonary hypertension, aiming to provide new ideas for the prevention and treatment of hypoxic pulmonary hypertension.