Suppr超能文献

弥漫性胶质瘤中的细胞衰老:从病理生理学到可能的治疗方法

Cellular Senescence in Diffuse Gliomas: From Physiopathology to Possible Treatments.

作者信息

Ordónez-Rubiano Edgar G, Cómbita Alba, Baldoncini Matías, Payán-Gómez César, Gómez-Amarillo Diego F, Hakim Fernando, Camargo Julián, Zorro-Sepúlveda Valentina, Luzzi Sabino, Zorro Oscar, Parra-Medina Rafael

机构信息

Department of Neurological Surgery, Fundación Universitaria de Ciencias de la Salud (FUCS), Hospital de San José - Sociedad de Cirugía de Bogotá, Bogotá, Colombia; School of Medicine, Universidad Nacional de Colombia, Bogotá, Colombia; Department of Neurosurgery, Hospital Universitario Fundación Santa Fe de Bogotá, Bogotá, Colombia.

Department of Neurosurgery, Hospital Universitario Fundación Santa Fe de Bogotá, Bogotá, Colombia; Department of Microbiology, Universidad Nacional de Colombia, Bogotá, Colombia.

出版信息

World Neurosurg. 2024 Nov;191:138-148. doi: 10.1016/j.wneu.2024.08.060. Epub 2024 Sep 2.

Abstract

Cellular senescence in gliomas is a complex process that is induced by aging and replication, ionizing radiation, oncogenic stress, and the use of temozolomide. However, the escape routes that gliomas must evade senescence and achieve cellular immortality are much more complex, in which the expression of telomerase and the alternative lengthening of telomeres, as well as the mutation of some proto-oncogenes or tumor suppressor genes, are involved. In gliomas, these molecular mechanisms related to cellular senescence can have a tumor-suppressing or promoting effect and are directly involved in tumor recurrence and progression. From these cellular mechanisms related to cellular senescence, it is possible to generate targeted senostatic and senolytic therapies that improve the response to currently available treatments and improve survival rates. This review aims to summarize the mechanisms of induction and evasion of cellular senescence in gliomas, as well as review possible treatments with therapies targeting pathways related to cellular senescence.

摘要

胶质瘤中的细胞衰老过程很复杂,它由衰老与复制、电离辐射、致癌应激以及替莫唑胺的使用所诱导。然而,胶质瘤逃避衰老并实现细胞永生化所必须的逃逸途径要复杂得多,其中涉及端粒酶的表达、端粒的替代性延长,以及一些原癌基因或肿瘤抑制基因的突变。在胶质瘤中,这些与细胞衰老相关的分子机制可产生抑瘤或促瘤作用,并直接参与肿瘤的复发和进展。从这些与细胞衰老相关的细胞机制出发,有可能产生靶向衰老抑制和衰老溶解疗法,从而改善对现有治疗的反应并提高生存率。本综述旨在总结胶质瘤中细胞衰老的诱导和逃避机制,并回顾针对与细胞衰老相关途径的可能治疗方法。

文献AI研究员

20分钟写一篇综述,助力文献阅读效率提升50倍。

立即体验

用中文搜PubMed

大模型驱动的PubMed中文搜索引擎

马上搜索

文档翻译

学术文献翻译模型,支持多种主流文档格式。

立即体验