Stromal interaction molecule 1 (STIM1) is a key component mediating store-operated calcium entry (SOCE), which controls the opening and closing of plasma membrane Ca 2+ channels by sensing the Ca 2+ content of endoplasmic reticulum luminal stores, and thus affects the processes of cell adhesion, migration, gene expression and proliferation. Studies have shown that STIM1 is abnormally expressed in a variety of cells such as neurons, endothelial cells and platelets during ischemic stroke (IS) development; it plays an important role in the pathological processes regulating hypertension, promoting thrombosis, activating cellular autophagy, mediating apoptosis and promoting neuroinflammation. This review summarizes the research progress of STIM1 in the development and prognostic assessment of IS, and seeks to provide theoretical references for potential therapeutic targets for IS.