摘要
背景:动脉粥样硬化是一种慢性炎性疾病,是几种重要心血管事件,特别是冠状动脉疾病和中风的主要危险因素。动脉粥样硬化的病理过程被认为是动态和复杂的,涉及动脉内各种不同细胞类型与迁移到血管壁的细胞之间的相互作用。 目的:E1A刺激基因(CREG)的人类细胞阻遏物最初被鉴定为具有拮抗由腺病毒E1A癌蛋白诱导的转录激活和细胞转化的能力的转录因子。然而,随后的研究也将其认定为能够维持细胞内稳态并能抵抗病理性细胞和组织损伤的分泌型糖蛋白。 结果:我们证实CREG可能调节血管壁细胞的体内平衡并抑制血管组织细胞和巨噬细胞的炎症,表明CREG对炎症有潜在的保护作用。在机械上,CREG表现得像典型的可溶性溶酶体蛋白质,其通过调节小GTP酶蛋白Rab7来调节溶酶体的形成和成熟,以介导血管组织细胞中的自噬。 结论:CREG对溶酶体形成的影响可能在动脉粥样硬化中具有重要的治疗意义。
关键词: 动脉粥样硬化,自噬,E1A刺激基因的细胞阻遏物,溶酶体,冠状动脉疾病,中风
图形摘要
Current Drug Targets
Title:Cellular Repressor of E1A-stimulated Genes, A New Potential Therapeutic Target for Atherosclerosis
Volume: 18 Issue: 15
关键词: 动脉粥样硬化,自噬,E1A刺激基因的细胞阻遏物,溶酶体,冠状动脉疾病,中风
摘要: Background: Atherosclerosis is a chronic inflammatory disease and a major risk factor for several important cardiovascular events, particularly coronary artery disease and stroke. The pathological process of atherosclerosis is considered to be dynamic and complicated, involving interactions between various different cell types within arteries and the cells that migrate into the vessel wall.
Objective: Human cellular repressor of E1A-stimulated genes (CREG) was originally identified as a transcription factor with the ability to antagonize transcriptional activation and cellular transformation induced by the adenovirus E1A oncoprotein. However, subsequent studies also identified it as a secreted glycoprotein able to sustain cellular homeostasis and withstand pathological cell and tissue damage.
Results: We demonstrated that CREG may modulate homeostasis of vascular wall cells and inhibit inflammation of vascular tissue cells and macrophages, indicating a potential protective effect of CREG against inflammation. Mechanistically, CREG behaves like a typical soluble lysosomal protein that regulates the formation and maturation of lysosomes by modulating the small GTPase protein Rab7, to mediate autophagy in vascular tissue cells.
Conclusion: The impact of CREG on lysosome formation may have important therapeutic significance in atherosclerosis.
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Cite this article as:
Cellular Repressor of E1A-stimulated Genes, A New Potential Therapeutic Target for Atherosclerosis, Current Drug Targets 2017; 18 (15) . https://dx.doi.org/10.2174/1389450117666161026111250
DOI https://dx.doi.org/10.2174/1389450117666161026111250 |
Print ISSN 1389-4501 |
Publisher Name Bentham Science Publisher |
Online ISSN 1873-5592 |
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