Stroke is an acute cerebrovascular disease that is caused by disruptions in the cerebral blood supply and leads to brain tissue damage. Its pathological mechanisms remain to be fully elucidated. Stroke has high incidence, disability, and mortality rates, thus substantially affecting life and health. Against this backdrop, intracellular mitochondria, which are central to cellular energy metabolism and crucial for cell survival, have major roles in ischemic stroke. Ischemic stroke results in brain cell oxygen and nutrient deprivation, thereby triggering oxidative stress and inflammatory reactions, impairing mitochondrial function, and disrupting energy metabolism. Mitochondrial autophagy is a protective mechanism to improve the quality and quantity of mitrochondria, and exerts neuroprotective effects. In recent years, preserving mitochondrial function after ischemic stroke has emerged as a major research topic. Increasing evidence suggests a close relationship between abnormal mitochondrial autophagy and the occurrence, progression, and pathophysiology of ischemic stroke. However, current research has not adequately explained how ischemic stroke regulates the initiation and execution of mitochondrial autophagy. Elucidating this mechanism in detail will be critical for understanding the development of stroke injury, and identifying novel and effective intervention strategies. Additionally, the optimal treatment time window must be determined to enable effective interventions in mitochondrial autophagy and minimize brain damage. To deepen understanding of mitochondrial autophagy, this review summarizes mitochondrial autophagy’s signaling pathways and its major role in ischemic stroke pathophysiology. Further exploration in this field will provide a crucial theoretical foundation for developing novel therapeutic strategies and clinical applications.