Abstract: Lacunar infarction (LI) and intracranial artery calcification (IAC) share multiple common vascular risk factors, including hypertension, diabetes mellitus, smoking, and advanced age, suggesting a potential shared pathophysiological basis. Emerging evidence indicates that IAC, beyond being a radiological marker of vascular aging, may contribute to LI pathogenesis through mechanisms such as inducing atherosclerotic stenosis at the ostia of perforating arteries, disrupting local hemodynamic homeostasis, and promoting microembolus formation. Substantial epidemiological and neuroimaging evidence demonstrates significant positive correlations of the presence and calcification burden of IAC with the risk of LI incidence, lesion count, and adverse clinical outcomes. This review systematically summarized the underlying molecular and hemodynamic mechanisms by which IAC mediates LI formation, presented population-based epidemiological data, and provided multimodal neuroimaging evidence. It also discussed the clinical implications of IAC in stroke subtyping, risk stratification, and individualized prevention strategies, and outlined future research directions.