2022 年2 期 第30 卷
新进展微量元素参与主动脉疾病发病机制的研究进展
Research Progress of Trace Elements in the Pathogenesis of Aortic Diseases
作者:邢凯,王志维
- 单位:
- 430060湖北省武汉市,武汉大学人民医院心血管外科
- Units:
- Department of Cardiovascular Surgery, Renmin Hospital of Wuhan University, Wuhan 430060, China
- 关键词:
- 主动脉疾病;主动脉瘤;主动脉夹层;微量元素;铁;锌;铜;硒
- Keywords:
- Aortic diseases; Aortic aneurysm; Aortic dissection; Trace elements; Iron; Zinc; Copper; Selenium
- CLC:
- R 543.1
- DOI:
- 10.12114/j.issn.1008-5971.2022.00.026
- Funds:
- 国家自然科学基金面上项目(82070481)
摘要:
研究表明,人体必需微量元素如铁、铜、锌、硒等在主动脉疾病如主动脉瘤和主动脉夹层患者体内 存在不同程度的紊乱。本文通过检索、分析相关文献,总结了微量元素参与主动脉疾病的发病机制,其中铁、铜过载 能够通过芬顿/哈伯-韦斯反应而产生过氧化物,进而对主动脉壁细胞造成氧化损伤;铁缺乏能够影响肌动蛋白的合成 和肌球蛋白的磷酸化,破坏细胞骨架和平滑肌收缩功能;铜缺乏能够抑制赖氨酰氧化酶(LOX)活性,影响胶原蛋白 和弹性蛋白的交联,破坏主动脉的抗张强度和弹性。锌、硒缺乏能够降低机体抗氧化能力,加重氧化损伤。此外,微 量元素紊乱还可以引起动脉组织的慢性炎症反应,激活c-Jun氨基端蛋白激酶(JNK)通路和核因子κB(NF-κB)通 路,进而增加基质金属蛋白酶(MMP)-2、MMP-9的表达,破坏细胞外基质。
Abstract:
It's demonstrated that essential trace elements (e.g., iron, copper, zinc, and selenium) have varying degrees of abnormalities in patients with aortic aneurysm or aortic dissection. By searching and analyzing the relevant literature, this paper summarizes the involvement of trace elements in the pathogenesis of aortic disease. The overload of iron and copper can result in oxidative damage to aortic tissue by the Fenton/Haber-Weiss reactions; iron deficiency can disrupt the cytoskeleton and inhibit the contractile function of smooth muscle by affecting the synthesis of actin and the level of myosin phosphorylation; copper deficiency can break the cross-linking of collagen and elastin by inhibiting the activity of lysyl oxidase (LOX) , ultimately destroying the tensile strength and elasticity of the aorta. And the oxidative damage can be aggravated by the lack of zinc and selenium. Furthermore, disorders of trace elements can also cause chronic inflammation in arterial tissue by the c-Jun N-terminal protein kinase (JNK) pathway and nuclear factor-к B (NF-κB) pathway, which increase the expression of matrix metalloproteinase (MMP)-2, MMP-9 to destroy the extracellular matrix.
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