刺激1
口腔1
细胞生物学
内质网
细胞质
钙信号传导
胞浆
跨膜蛋白
细胞外
生物学中的钙
钙
细胞内
化学
生物
生物化学
受体
有机化学
酶
作者
Xueqi Wan,Jinfan Tian,Peng Hao,Kun Zhou,Jing Zhang,Yuquan Zhou,Chang-Jiang Ge,Xiantao Song
出处
期刊:Aging and Disease
[Aging and Disease]
日期:2022-01-01
卷期号:13 (6): 1606-1606
被引量:1
标识
DOI:10.14336/ad.2022.0417
摘要
The important role of Ca2+ in pathogenic store-operated calcium entry (SOCE) is well-established. Among the proteins involved in the calcium signaling pathway, Stromal interacting molecule 1 (STIM1) is a critical endoplasmic reticulum transmembrane protein. STIM1 is activated by the depletion of calcium stores and then binds to another calcium protein, Orai1, to form a channel through which the extracellular Ca2+ can enter the cytoplasm to replenish the calcium store. Multiple studies have shown that increased STIM1 facilitates the aberrant proliferation and apoptosis of vascular smooth cells (VSMC) and macrophages which can promote the formation of rupture-prone plaque. Together with regulating the cytosolic Ca2+ concentration, STIM1 also activates STING through altered intracellular Ca2+ concentration, a critical pro-inflammatory molecule. The cGAS-STING pathway is linked with cellular proliferation and phenotypic conversion of VSMC and enhances the progression of atherosclerosis plaque. In summary, we conclude that STIM1/cGAS-STING is involved in the progression of AS and plaque vulnerability.
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