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维生素 D 缺乏与儿童 1 型糖尿病发病关系的研究进展。

Progress in the Relationship between Vitamin D Deficiency and the Incidence of Type 1 Diabetes Mellitus in Children.

机构信息

School of Medicine, Taizhou University, Jiaojiang, 318000 Zhejiang, China.

Children's Hospital of Nanjing Medical University, Nanjing, 210008 Jiangsu, China.

出版信息

J Diabetes Res. 2022 Sep 2;2022:5953562. doi: 10.1155/2022/5953562. eCollection 2022.

Abstract

Type 1 diabetes mellitus (T1DM) is an autoimmune disease, due to a large number of islet cells damaged, resulting in an absolute lack of insulin, ultimately relying on insulin therapy. Vitamin D is a fat-soluble sterol derivative that not only participates in calcium and phosphorus metabolism but also acts as an immunomodulatory role by binding to nuclear vitamin D receptors to regulate the expression of transcription factors. Increasing evidence has shown that vitamin D has immunoregulation and anti-inflammatory effects, and it may play a role in T cell regulatory responses due to downregulation in the expression of cathepsin G and inhibition of CD4+ T cell activation and protection of cells from immune attack and is beneficial in decreasing oxidative stress in T1DM patients. Epidemiologic evidence demonstrates involvement of vitamin D deficiency in T1DM pathogenesis, with the immune system improperly targeting and destroying its own islet cells. In addition, polymorphisms in genes critical for vitamin D metabolism may increase the risk of islet autoimmunity and T1DM. In this paper, the relationship between vitamin D deficiency and the molecular mechanism of T1DM was discussed.

摘要

1 型糖尿病(T1DM)是一种自身免疫性疾病,由于大量胰岛β细胞受损,导致胰岛素绝对缺乏,最终依赖胰岛素治疗。维生素 D 是一种脂溶性甾醇衍生物,不仅参与钙磷代谢,还通过与核维生素 D 受体结合发挥免疫调节作用,调节转录因子的表达。越来越多的证据表明,维生素 D 具有免疫调节和抗炎作用,由于组织蛋白酶 G 的表达下调以及抑制 CD4+T 细胞的激活和保护β细胞免受免疫攻击,其可能在 T 细胞调节反应中发挥作用,从而有利于减少 T1DM 患者的氧化应激。流行病学证据表明,维生素 D 缺乏与 T1DM 的发病机制有关,免疫系统错误地靶向和破坏自身的胰岛β细胞。此外,维生素 D 代谢关键基因的多态性可能会增加胰岛自身免疫和 T1DM 的风险。本文讨论了维生素 D 缺乏与 T1DM 发病机制的分子机制之间的关系。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/435b/9463035/087ca824cd6e/JDR2022-5953562.001.jpg

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