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作 者:刘禹杉 杨树森 张仪霖 李京涛 闫曙光[1] LIU Yushan;YANG Shusen;ZHANG Yilin;LI Jingtao;YAN Shuguang(College of Basic Medicine,Shaanxi University of Chinese Medicine,Xianyang 712046,China;Department of Hepatology,afiliated Hospital of Shaanxi University of Chinese Medicine,Xianyang 712000,China)
机构地区:[1]陕西中医药大学基础医学院,陕西咸阳712046 [2]陕西中医药大学附属医院肝病科,陕西咸阳712000
出 处:《海南医科大学学报》2025年第1期73-80,共8页Journal of Hainan Medical University
基 金:国家自然科学基金资助项目(81873233、82174330);陕西中医药大学科技创新团队(2023-CXTD-01)。
摘 要:慢性炎症、损伤和修复的反复恶性循环引起纤维化疾病的发生。越来越多的证据表明,组织损伤能够通过激活上皮-间充质转化(epithelial to mesenchymal transition,EMT)的方式促进纤维化进展,包括活化成纤维细胞、促进细胞迁移、侵袭以及加速细胞外基质的过度累积等。近来的研究发现钙库操纵性钙内流(store-operated calcium entry,SOCE)可促进EMT加剧纤维化疾病,通过抑制其信号转导具有防治纤维化的作用,其中,抗衰老蛋白Klotho可能存在调控SOCE进而防治纤维化疾病的作用。基于此,本文就近年来关于SOCE在纤维化疾病中对EMT的控制作用以及Klotho可能存在的调控作用进行简要综述,以期为进一步研究提供理论支持。The development of fibrotic diseases is often attributed to a recurrent cycle of chronic inflammation,injury,and re-pair.Growing evidence suggests that tissue injury can promote fibrosis progression by activating epithelial to mesenchymal transi-tion(EMT),which involves fibroblast activation,cell migration and invasion,as well as excessive accumulation of extracellular matrix.Recent studies have shown that store-operated calcium entry(SOCE)promotes EMT and worsens fibrotic diseases,while inhibiting its signaling can help prevent and control fibrosis.In this context,the anti-aging protein Klotho may play a regulatory role in preventing and controlling fibrotic diseases by regulating SOCE.Therefore,this paper aims to review recent studies on the role of SOCE in regulating EMT in fibrotic diseases,as well as the potential regulatory function of Klotho,in order to offer theo-retical support for future research.
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