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缺氧驱动的血管肿瘤血管生成与代谢重编程

Hypoxia-driven angiogenesis and metabolic reprogramming in vascular tumors.

作者信息

Liu Lu, Yu Jiayun, Liu Yang, Xie Liang, Hu Fan, Liu Hanmin

机构信息

Department of Pediatric Pulmonology and Immunology, West China Second University Hospital, Sichuan University, Chengdu, China.

Key Laboratory of Birth Defect and Related Diseases of Women and Children (Sichuan University), Ministry of Education, Chengdu, Sichuan, China.

出版信息

Front Cell Dev Biol. 2025 May 15;13:1572909. doi: 10.3389/fcell.2025.1572909. eCollection 2025.

Abstract

Hypoxia is a hallmark of the tumor microenvironment (TME), and it plays a crucial role in the occurrence and progression in vascular tumors. Under hypoxic conditions, hypoxia-inducible factor 1-alpha (HIF-1α) is stabilized, inducing changes in the expression of various target genes involved in angiogenesis, metabolism, and cell survival. This includes the upregulation of pro-angiogenic factors like VEGF, which promotes the formation of dysfunctional blood vessels, contributing to the worsening of the hypoxic microenvironment. At the same time, hypoxia induces a metabolic shift toward glycolysis, even in the presence of oxygen, supporting tumor cell survival and proliferation by providing necessary energy and biosynthetic precursors. This review discusses the molecular mechanisms by which hypoxia regulates angiogenesis and metabolic reprogramming in vascular tumors, highlighting the intricate link between these processes, and explores potential therapeutic strategies to target these pathways in order to develop effective treatment strategies for patients.

摘要

缺氧是肿瘤微环境(TME)的一个标志,在血管肿瘤的发生和发展中起着关键作用。在缺氧条件下,缺氧诱导因子1α(HIF-1α)会稳定下来,诱导参与血管生成、代谢和细胞存活的各种靶基因的表达发生变化。这包括促血管生成因子如VEGF的上调,VEGF促进功能失调血管的形成,导致缺氧微环境恶化。同时,缺氧诱导代谢向糖酵解转变,即使在有氧的情况下也是如此,通过提供必要的能量和生物合成前体来支持肿瘤细胞的存活和增殖。本综述讨论了缺氧调节血管肿瘤中血管生成和代谢重编程的分子机制,强调了这些过程之间的复杂联系,并探索了针对这些途径的潜在治疗策略,以便为患者制定有效的治疗方案。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7a5d/12119610/003e1ce710f4/fcell-13-1572909-g001.jpg

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