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代谢重编程与血管生成干预

Metabolic reprogramming and interventions in angiogenesis.

作者信息

Liu Yun, Wu Zifang, Li Yikun, Chen Yating, Zhao Xuan, Wu Miaomiao, Xia Yaoyao

机构信息

College of Animal Science and Technology, Southwest University, Chongqing 400715, China.

College of Animal Science and Technology, Northwest A&F University, Yangling, Shaanxi 712100, China.

出版信息

J Adv Res. 2025 Apr;70:323-338. doi: 10.1016/j.jare.2024.05.001. Epub 2024 May 3.

DOI:10.1016/j.jare.2024.05.001
PMID:38704087
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11976431/
Abstract

BACKGROUND

Endothelial cell (EC) metabolism plays a crucial role in the process of angiogenesis. Intrinsic metabolic events such as glycolysis, fatty acid oxidation, and glutamine metabolism, support secure vascular migration and proliferation, energy and biomass production, as well as redox homeostasis maintenance during vessel formation. Nevertheless, perturbation of EC metabolism instigates vascular dysregulation-associated diseases, especially cancer.

AIM OF REVIEW

In this review, we aim to discuss the metabolic regulation of angiogenesis by EC metabolites and metabolic enzymes, as well as prospect the possible therapeutic opportunities and strategies targeting EC metabolism.

KEY SCIENTIFIC CONCEPTS OF REVIEW

In this work, we discuss various aspects of EC metabolism considering normal and diseased vasculature. Of relevance, we highlight that the implications of EC metabolism-targeted intervention (chiefly by metabolic enzymes or metabolites) could be harnessed in orchestrating a spectrum of pathological angiogenesis-associated diseases.

摘要

背景

内皮细胞(EC)代谢在血管生成过程中起着至关重要的作用。糖酵解、脂肪酸氧化和谷氨酰胺代谢等内在代谢事件,在血管形成过程中支持安全的血管迁移和增殖、能量和生物量的产生以及氧化还原稳态的维持。然而,内皮细胞代谢的紊乱会引发与血管失调相关的疾病,尤其是癌症。

综述目的

在本综述中,我们旨在讨论内皮细胞代谢物和代谢酶对血管生成的代谢调节,并展望针对内皮细胞代谢的可能治疗机会和策略。

综述的关键科学概念

在这项工作中,我们考虑正常和病变脉管系统,讨论内皮细胞代谢的各个方面。相关的是,我们强调内皮细胞代谢靶向干预(主要通过代谢酶或代谢物)的意义可用于协调一系列与病理性血管生成相关的疾病。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f183/11976431/7a5694e7ea07/gr5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f183/11976431/0658b8e6369e/ga1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f183/11976431/975ae23b8c3d/gr1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f183/11976431/8859b72433d1/gr2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f183/11976431/41f1abe1ecde/gr3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f183/11976431/f4989daa6fac/gr4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f183/11976431/7a5694e7ea07/gr5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f183/11976431/0658b8e6369e/ga1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f183/11976431/975ae23b8c3d/gr1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f183/11976431/8859b72433d1/gr2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f183/11976431/41f1abe1ecde/gr3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f183/11976431/f4989daa6fac/gr4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f183/11976431/7a5694e7ea07/gr5.jpg

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Recombinant chromosome 6 open reading frame 120 protein promotes angiogenesis and endothelial‑to‑mesenchymal transition in human umbilical vein endothelial cells via the PI3K/Akt signaling pathway.重组6号染色体开放阅读框120蛋白通过PI3K/Akt信号通路促进人脐静脉内皮细胞的血管生成和内皮-间充质转化。
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Transl Oncol. 2025 Jul;57:102402. doi: 10.1016/j.tranon.2025.102402. Epub 2025 May 2.
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