Vascular cognitive impairment (VCI), a syndrome induced by cerebrovascular disease and its risk factors, has become a major public health challenge worldwide. Especially in the context of an increasingly aging population, its impact is becoming more significant. In recent years, research has gradually revealed the crucial role of chronic cerebral hypoperfusion (CCH) in the occurrence and development of VCI. CCH leads to long-term ischemia and hypoxia in brain tissue, which seriously threatens mitochondrial function and triggers a series of problems such as mitochondrial oxidative stress, calcium homeostasis disturbance, dynamic abnormalities, autophagy dysregulation, and impaired biogenesis. These issues are extensively involved in the pathological process of VCI. This article provides an overview of the correlation between mitochondrial dysfunction and VCI under CCH conditions, aiming to explore new directions for the treatment of VCI.
