基质相互作用分子1（STIM1）是钙池操纵性钙内流（SOCE）的关键成分，通过感知内质网腔内存储Ca2+含量以控制质膜Ca2+通道的开放与关闭，进而影响细胞粘附、迁移、基因表达和增殖等过程。研究表明，在缺血性脑卒中（IS）的发生发展过程中，STIM1在神经元、内皮细胞和血小板等多种细胞中表达异常，在高血压调控以及促进血栓形成、激活细胞自噬、介导细胞凋亡和促进神经炎症的病理过程中发挥重要作用。本文对STIM1在IS发生发展和预后评估中的研究进展进行总结，力求为寻找IS的潜在治疗靶点提供理论参考。 Stromal interaction molecule 1 (STIM1) is a key component mediating store-operated calcium entry (SOCE)， which controls the opening and closing of plasma membrane Ca2+ channels by sensing the Ca2+ 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。
Recent advance in role of stromal interaction molecule 1 in ischemic stroke
Stromal interaction molecule 1 (STIM1) is a key component mediating store-operated calcium entry (SOCE), which controls the opening and closing of plasma membrane Ca2+ channels by sensing the Ca2+ 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.
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