%0 Journal Article %T 白细胞介素4诱导蛋白1在神经胶质瘤中的调节作用及研究进展
Regulatory Role of Interleukin 4-Inducible Protein 1 in Glioma and Research Progress %A 齐新 %A 韩光魁 %J Journal of Clinical Personalized Medicine %P 808-814 %@ 2334-3443 %D 2025 %I Hans Publishing %R 10.12677/jcpm.2025.42246 %X 神经胶质瘤是一种常见、具有高度侵袭性的神经系统肿瘤,因生长快速,广泛浸润邻近脑组织,假性坏死和诱导血管生成,且无明显的作用靶点,所以胶质瘤预后较差,复发率高,其发生和发展受到多种细胞因子的调节。其中白细胞介素4诱导蛋白1 (IL-4I1)作为一种重要的神经系统细胞因子,逐渐引起了研究者的关注。IL-4I1不仅参与肿瘤微环境的调节,还可能影响肿瘤细胞的增殖、存活和迁移等过程,在神经胶质瘤的发生与发展中发挥重要作用。目前的研究表明,IL-4I1通过多条信号通路影响神经胶质瘤的生物学特性,但其具体机制还未有明确说明。因此,通过影响IL-4I1的表达为神经胶质瘤的治疗提供了新的思路。本文旨在综述IL-4I1在神经胶质瘤中的作用机制、相关信号通路以及其在临床应用中的前景,为研究人员提供关于IL-4I1在这一领域的最新进展和未来研究方向。
Glioma is a common and highly aggressive neurologic tumor with a poor prognosis and high recurrence rate due to its rapid growth, extensive invasion of adjacent brain tissues, pseudonecrosis and induction of angiogenesis, and no obvious target, and its occurrence and progression are regulated by a variety of cytokines. Among them, interleukin 4-inducible protein 1 (IL-4I1), as an important nervous system cytokine, has gradually attracted the attention of researchers. IL-4I1 is not only involved in the regulation of tumor microenvironment, but also may affect the proliferation, survival and migration of tumor cells, and plays an important role in the occurrence and development of glioma. Current studies have shown that IL-4I1 affects the biology of glioma through multiple signaling pathways, but the specific mechanism of IL-4I1 has not been clearly explained. Therefore, by affecting the expression of IL-4I1, it provides a new idea for the treatment of glioma. The purpose of this article is to review the mechanism of IL-4I1 in glioma, related signaling pathways, and its prospects for clinical application, and to provide researchers with the latest progress and future research directions of IL-4I1 in this field. %K 白细胞介素4诱导蛋白1, %K 神经胶质瘤, %K 细胞因子, %K 信号通路, %K 临床应用
IL-4I1 %K Glioma %K Cytokines %K Signaling Pathways %K Clinical Applications %U http://www.hanspub.org/journal/PaperInformation.aspx?PaperID=111247