Intracerebral hemorrhage (ICH) is a severe, life-threatening subtype of stoke that constitutes a crucial health and socioeconomic problem worldwide. However, the current clinical treatment can only reduce the mortality of patients to a certain extent, but cannot ameliorate neurological dysfunction and has a high recurrence rate. Increasing evidence has demonstrated that mitochondrial dysfunction occurs in the early stages of brain injury and participates in all stages of secondary brain injury (SBI) after ICH. As the energy source of cells, various pathobiological processes that lead to SBI closely interact with the mitochondria, such as oxidative stress, calcium overload, and neuronal injury. In this review, we discussed the structure and function of mitochondria and the abnormal morphological changes after ICH. In addition, we discussed recent research on the involvement of mitochondrial dynamics in the pathological process of SBI after ICH and introduced the pathological variations and related molecular mechanisms of mitochondrial dysfunction in the occurrence of brain injury. Finally, we summarized the latest progress in mitochondrion-targeted agents for ICH, which provides a direction for the development of emerging therapeutic strategies targeting the mitochondria after ICH.